shock and hemorrhage
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TRANSCRIPT
Benjamin Pace, MD, FACSDirector of Surgery
Queens Hospital CenterAssociate Professor of SurgeryMount Sinai School of Medicine
Hemorrhage and Shock
Acknowledgements
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Defining Shock (1 of 2)
Shock is best defined as inadequate tissue perfusion. 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.
“The rude unhinging of the machinery of Life”
Gross, 1877
Defining Shock (2 of 2)
Shock is not adequately defined by: Pulse rate Blood pressure Cardiac function Hypovolemia Loss of systemic vascular resistance
Hemorrhage Classification
External Hemorrhage
Accounts for nearly 10 million emergency department visits in the United States each year.
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
Internal hemorrhage is associated with higher
morbidity and mortality than external hemorrhage.
Physiological Response to Hemorrhage The body’s initial response to
hemorrhage is to stop bleeding by chemical means (hemostasis). This vascular reaction involves:
Local vasoconstriction Formation of a platelet plug Coagulation Growth of tissue into the blood clot that
permanently closes and seals the injured vessel
Hemorrhage Control
External Hemorrhage Direct pressure and pressure dressing General Management
Direct pressure Elevation Ice Pressure points Constricting band Tourniquet
May use a BP cuff by inflating the cuff 20–30 mmHg above the SBP
Release may send toxins to heart Lactic acid and electrolytes
Tourniquets are ONLY used as a last resort!
Internal Hemorrhage Control
Hematoma Pocket of blood
between muscle and fascia
UNEXPLAINED SHOCK is BEST attributed to abdominal trauma
General Management Immobilization,
stabilization, elevation
Epistaxis: Nose Bleed Causes: trauma,
hypertension Treatment: lean forward,
pinch nostrils Hemoptysis Esophageal Varices Melena Diverticulosis Chronic Hemorrhage
Anemia
Stages of Hemorrhage
60% of body weight is fluid. 7% circulating blood volume (CBV) in
men 5 L (10 units)
6.5% CBV in women 4.6 L (9–10 units)
Stages of Hemorrhage Stage 1 15% loss of CBV
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
Class I
acute hemorrhage
Treatment of Stage 1 Hemorrhage
Ringer’s lactate solution via large bore IVs
Identify and Control the Source of Bleeding
Stages of Hemorrhage Stage 2 15–25% loss of CBV
750–1250 mL Early decompensation
Unable to maintain BP Tachycardia and tachypnea
Stages of Hemorrhage Stage 2 (2 of 2)
Decreased pulse strength Narrowing pulse pressure Significant catecholamine release
Increased Peripheral Vascular Resistance Cool, clammy skin and thirst Increased anxiety and agitation Normal renal output
Class II
acute hemorrhage
Treatment of Stage 2 Hemorrhage
Ringer’s lactate solution via large bore IVs
Typed and Cross matched Blood Identify and Control the Source of
Bleeding
Stages of Hemorrhage Stage 3 25–35% loss of CBV
1250–1750 mL Late decompensation (early
irreversible) Compensatory mechanisms unable to
cope with loss of blood volume
Stages of Hemorrhage Stage 3 Classic Shock
Weak, thready, rapid pulse Narrowing pulse pressure
Tachypnea Anxiety, restlessness Decreased Level of Conciousness Pale, cool, and clammy skin
Class IIIacute hemorrhage
Treatment of Stage 2 Hemorrhage
Ringer’s lactate solution via large bore IVs
Typed Specific or O neg Blood Identify and Control the Source of
Bleeding
Stages of Hemorrhage Stage 4 >35% 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
Class IV
acute hemorrhage
Treatment of Stage 2 Hemorrhage
Ringer’s lactate solution via large bore IVs
O neg Blood
Identify and Control the Source of Bleeding
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
Stages of Hemorrhage Concomitant Factors Children
CBV 8–9% of body weight Poor compensatory mechanisms TREAT AGGRESIVELY!
Elderly Decreased CBV Medications
BP Anticoagulants
Hemorrhage Assessment
Initial Assessment General Impression
Obvious Bleeding Mental Status
Interventions Manage as you go:
O2
Bleeding control Tx Shock
Hemorrhage Assessment (4 of 5)
Fractures and Possible Blood Loss
Pelvic fracture: Femur fracture: Tibia/fibula fracture: Hematomas and
contusions:
2,000 mL1,500 mL500–750 mL500 mL
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
SHOCK is…INADEQUATE TISSUEPERFUSION.
Stages of ShockCellular Level
Four Stages
Stage 1: Vasoconstriction Stage 2: Capillary and venule
opening Stage 3: Disseminated intravascular
coagulation Stage 4: Multiple organ failure
Stage 1: Vasoconstriction (1 of 4)
Vasoconstriction begins as minimal perfusion to capillaries continues. Oxygen and substrate delivery to the
cells supplied by these capillaries decreases.
Anaerobic metabolism replaces aerobic metabolism.
Stage 1: Vasoconstriction (2 of 4)
Production of lactate and hydrogen ions increases. The lining of the capillaries may begin to
lose the ability to retain large molecular structures within its walls.
Protein-containing fluid leaks into the interstitial spaces (leaky capillary syndrome).
Stage 1: Vasoconstriction (3 of 4)
Sympathetic stimulation produces: Pale, sweaty skin Rapid, thready pulse Elevated blood glucose levels
The release of epinephrine dilates coronary, cerebral, and skeletal muscle arterioles and constricts other arterioles. Blood is shunted to the heart, brain, skeletal
muscle, and capillary flow to the kidneys and abdominal viscera decreases.
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.
Stage 2: Capillary and Venule Opening (1 of 5)
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.
Stage 2: Capillary and Venule Opening (2 of 5)
As the syndrome continues, the precapillary sphincters relax with some expansion of the vascular space.
Postcapillary sphincters resist local effects and remain closed, causing blood to pool or stagnate in the capillary system, producing capillary engorgement.
Stage 2: Capillary and Venule Opening (3 of 5)
As increasing hypoxemia and acidosis lead to opening of additional venules and capillaries, the vascular space expands greatly. Even normal blood volume may be
inadequate to fill the container. The capillary and venule capacity may
become great enough to reduce the volume of available blood for the great veins and vena cava. Resulting in decreased venous return and a
fall in cardiac output.
Stage 2: Capillary and Venule Opening (4 of 5)
Low arterial blood pressure and many open capillaries result in stagnant capillary flow.
Sluggish blood flow and the reduced delivery of oxygen result in increased anaerobic metabolism and the production of lactic acid. The respiratory system attempts to
compensate for the acidosis by increasing ventilation to blow off carbon dioxide.
Stage 2: Capillary and Venule Opening (5 of 5)
As acidosis increases and pH falls, the RBCs may cluster together (rouleaux formation). Halts perfusion Affects nutritional flow and prevents removal of
cellular metabolites
Clotting mechanisms are also affected, leading to hypercoagulability.
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.
Stage 3: Disseminated Intravascular Coagulation (DIC) (1 of 4) Time of onset will depend on degree of
shock, patient age, and pre-existing medical conditions.
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.
Stage 3: Disseminated Intravascular Coagulation (DIC) (2 of 4) Stage 3 is resistant to treatment
(refractory shock), but is still reversible.
Blood begins to coagulate in the microcirculation, clogging capillaries. Capillaries become occluded by clumps of
RBCs. Decreases capillary perfusion and prevents
removal of metabolites Distal tissue cells use anaerobic
metabolism, and lactic acid production increases.
Stage 3: Disseminated Intravascular Coagulation (DIC) (3 of 4)
Lactic acid accumulates around the cell. Cell membranes no longer have the
energy needed to maintain homeostasis.
Water and sodium leak in, potassium leaks out, and the cells swell and die.
Stage 3: Disseminated Intravascular Coagulation (DIC) (4 of 4)
Pulmonary capillaries become permeable, leading to pulmonary edema. Decreases the absorption of oxygen and
results in possible alterations in carbon dioxide elimination
May lead to acute respiratory failure or adult respiratory distress syndrome (ARDS)
If shock and disseminated intravascular coagulation (DIC) continue, the patient progresses to multiple organ failure.
Stage 4: Multiple Organ Failure (1 of 2)
The amount of cellular necrosis required to produce organ failure varies with each organ and the underlying condition of the organ. Usually hepatic failure occurs, followed by renal
failure, and then heart failure. If capillary occlusion persists for more than 1 to 2
hours, the cells nourished by that capillary undergo changes that rapidly become irreversible.
In this stage, blood pressure falls dramatically (to levels of 60 mmHg or less). Cells can no longer use oxygen, and metabolism
stops.
Stage 4: Multiple Organ Failure (2 of 2)
If a critical amount of the vital organ is damaged by cellular necrosis, the organ soon fails. Failure of the liver is common and often presents
early. Capillary blockage may cause heart failure. GI bleeding and sepsis may result from GI mucosal
necrosis. Pancreatic necrosis may lead to further clotting
disorders and severe pancreatitis. Pulmonary thrombosis may produce
hemorrhage and fluid loss into the alveoli. Leading to death from respiratory failure.
Hemorrhagic Shock Management
Hemorrhagic Shock Management
INTRAVENOUS FLUIDS AND BLOOD
IDENTIFY AND CONTROL THE SOURCE OF THE BLEEDING
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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
Specific Wound Considerations (2 of 2) 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
Transport Considerations
Consider rapid transport to Level I Ctr: Suspected serious blood loss Suspected serious internal bleeding Decompensating shock
AMS, pulse, narrowing pulse pressure WHEN IN DOUBT, TRANSPORT.
Other Considerations Sympathetic response Anxiety
Shock Management (1 of 2)
Airway and Breathing NRB PPV (overdrive respiration) ET CPAP PEEP
Hemorrhage Control Fluid Resuscitation
Catheter size and length Large bore 20 mL/kg of NS or LR Polyhemoglobins 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.
Shock Management (2 of 2)
Temperature Control Conserve core temperature Warm IV fluids
PASG Action
Increase PVR Reduce vascular volume Increase central CBV Immobilize lower extremities
Assess Pulmonary edema Pregnancy Vital signs
Hemorrhagic Shock Management Simultaneous with the ABCDE of
Advanced Trauma Life Support Decisions for interventions/surgery
as outlined for ATLS
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Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Topics Introduction to Hemorrhage and
Shock Hemorrhage Shock
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Introduction to Hemorrhage and Shock Hemorrhage
Abnormal internal or external loss of blood
Homeostasis Tendency of the body to maintain a
steady and normal internal environment Shock
INADEQUATE TISSUE PERFUSION Transition between homeostasis and
death
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Hemorrhage
Circulatory System Hemorrhage Classification Clotting Factors Affecting Clotting Hemorrhage Control Stages of Hemorrhage Hemorrhage Assessment Hemorrhage Management
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Cardiac Anatomy
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Heart
Cardiac Cycle The repetitive pumping action that
produces pressure changes that circulate blood throughout the body
Cardiac Output The total amount of blood separately
pumped by each ventricle per minute, usually expressed in liters per minute
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Cardiac Output
Normal cardiac output = 5 to 6 liters per minute (LPM).
Can increase up to 30 LPM in times of stress or exercise.
Determined by multiplying the heart rate by the volume of blood ejected by each ventricle during each beat (stroke volume).
CO is influenced by: Strength of contraction Rate of contraction Amount of venous return available to the
ventricle (preload)
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Circulatory System (1 of 4)
Heart Autonomic nervous system
Parasympathetic nervous system Slows rate Mediated by vagus nerve
Sympathetic nervous system Increases rate Cardiac plexus
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Circulatory System (2 of 4)
Key Terms Stroke Volume Preload Ventricular Filling Starling’s Law of the heart Afterload (End Diastolic Pressure or
EDP) Cardiac Output
SV x HR 5 liters/minute
Fick Principle
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Circulatory System (3 of 4)
Arteries Tunica Adventitia Tunica Media Tunica Intima
Arteriole Capillary: 7% of total blood volume Venule Vein
Constriction returns 20% (1 liter) of blood to active circulation
} 64% of blood volume
} 13% of blood volume
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Circulatory System (4 of 4)
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Cardiac Physiology
Vena Cavaand
SystemicVeins
Aortaand
SystemicArteries
SystemicCapillaries
PulmonaryArteries
LUNGS
PulmonaryVeins
RightAtrium
RightVentricle
LeftAtrium
LeftVentricle
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Circulation (1 of 2)
Systolic Pressure Strength and volume of cardiac output
Diastolic Pressure More indicative of the state of
constriction of the arterioles Mean Arterial Pressure
1/3 pulse pressure added to the diastolic pressure
Tissue perfusion pressure
Circulation (2 of 2)
Vascular Control Increased sympathetic tone results in
increased vasoconstriction. Microcirculation
Blood flow in the arterioles, capillaries, and venules.
Sphincter functioning. Most organ tissue requires blood flow
5 to 20% of the time.
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Cardiac Physiology (1 of 2)
Oxygen Supply The myocardium receives its blood/oxygen
supply during the diastole phase of contraction. The blood flows from the aorta through the two coronaries into the relaxed myocardium.
Oxygen Demand 90% of the O2 demand, or work, of the heart
is performed during the isovolumetric phase of contraction. In this phase, NO blood flows from the heart into the aorta, until the pressure in the heart is greater than the end diastolic pressure (EDP).
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Cardiac Physiology (2 of 2)
Releases a polypeptide called atrial natriuretic peptide (ANP)
Works antagonistically to renin-angiotensin
Four Effects Promotes Na+ and water loss at the kidneys Inhibits renin release and ADH, aldosterone
secretion Suppresses thirst Blocks action of angiotensin II and
norepinephrine
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Negative Feedback
Important negative feedback mechanisms in maintaining tissue perfusion are the: Baroreceptor reflexes Central nervous system ischemia
responses Hormonal mechanisms Reabsorption of tissue fluids
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Cardiovascular System Regulation PNS and SNS always act in balance Baroreceptors: monitor BP Chemoreceptors Hormone regulation Reabsorption of tissue fluids
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Cardiovascular System Regulation (2 of 3)
Parasympathetic Nervous System Decrease
Heart rate Strength of contractions Blood pressure
Increase Digestive system Kidneys
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Cardiovascular System Regulation (3 of 3)
Sympathetic Nervous System Increase
Body activity Heart rate Strength of contractions Vascular constriction
Bowel and digestive viscera Decreased urine production
Respirations Bronchodilation
Increases skeletal muscle perfusion
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Baroreceptor Reflexes (1 of 5)
High in the neck, each carotid artery divides into external and internal carotid arteries. At the bifurcation, the wall of the artery is
thin and contains many vine-like nerve endings.
The small portion of the artery is the carotid sinus. Nerve endings in this area are sensitive to
stretch or distortion. Serve as pressure receptors or baroreceptors.
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Baroreceptor Reflexes (2 of 5)
Similar area found in the arch of the aorta. Serves as a second important baroreceptor
Large arteries, large veins, and the wall of the myocardium also contain less important baroreceptors.
Baroreceptor reflexes help maintain blood pressure by two negative feedback mechanisms: By lowering blood pressure in response to
increased arterial pressure By increasing blood pressure in response to
decreased arterial pressure
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Baroreceptor Reflexes (3 of 5)
Normal blood pressure partially stretches the arterial walls so that baroreceptors produce a constant, low-frequency stimulation.
Impulses from the baroreceptors inhibit the vasoconstrictor center of the medulla and excite the vagal center when blood pressure increases. Results in vasodilation in the peripheral
circulatory system and a decrease in the heart rate and force of contraction. Combined effect is a decrease in arterial pressure.
Baroreceptor Reflexes (4 of 5)
Baroreceptors adapt in 1 to 3 days to whatever pressure level they are exposed. Therefore, they do not change the average blood pressure on a long-term basis. This adaptation is common in people who have chronic hypertension.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Baroreceptor Reflexes (5 of 5)
When baroreceptor stimulation ceases due to a fall in arterial pressure, several cardiovascular responses are evoked: Vagal stimulation is reduced and
sympathetic response is increased. The increase in sympathetic impulses
results in increased peripheral resistance and an increase in heart rate and stroke volume. Sympathetic discharges also produce generalized
arteriolar vasoconstriction, which decreases the container size.Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma
© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
The vasoconstriction in peripheral vascular beds results in the characteristic pale, cold skin of patients suffering from hypovolemic shock.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Chemoreceptor Reflexes
Chemoreceptors Monitor level of CO2 in CSF
Monitor level of O2 in blood
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Chemoreceptor Physiology
Low arterial pressure leads to hypoxemia and/or acidosis.
Hypoxemia/acidosis stimulate peripheral chemoreceptor cells within the carotid and aortic bodies. These bodies have an abundant blood
supply. When oxygen or pH decreases, these
cells stimulate the vasomotor center of the medulla. The rate and depth of ventilation are also
increased to help eliminate excess carbon dioxide and maintain acid-base balance.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
CV System and Hormone Regulation (1 of 7)
Catecholamines Epinephrine Norepinephrine Actions
Alpha 1 Alpha 2 Beta 1 Beta 2
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CV System and Hormone Regulation (2 of 7)
Alpha 1 Vasoconstriction Increased
peripheral vascular resistance
Increased preload Alpha 2
Regulates release of NE
Beta 1 Positive inotropy Positive
chronotropy Positive
dromotropy Beta 2
Bronchodilation Smooth muscle
dilation in bowel
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CV System and Hormone Regulation (3 of 7)
Antidiuretic Hormone (ADH) AKA: 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
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
CV System and Hormone Regulation (4 of 7)
Angiotensin II Released
Primary chemical from kidneys Lowered BP and decreased perfusion
Action Converted from renin into angiotensin I
Modified in lungs to angiotensin II 20-minute process Potent systemic vasoconstrictor 1-hour duration Causes release of ADH, aldosterone, and
epinephrine
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CV System and Hormone Regulation (5 of 7)
Aldosterone Release
Adrenal cortex Stimulated by angiotensin II
Action Maintain kidney ion balance Retention of sodium and water Reduce insensible fluid loss
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CV System and Hormone Regulation (6 of 7)
Glucagon Release
Alpha cells of pancreas Triggered by epinephrine
Action Causes liver and skeletal muscles to
convert glycogen into glucose Gluconeogenesis
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CV System and Hormone Regulation (7 of 7)
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
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Reabsorption of Tissue Fluids (1 of 2)
Arterial hypotension, arteriolar constriction, and reduced venous pressure during hypovolemia lower the blood pressure in the capillaries (hydrostatic pressure).
The decrease promotes reabsorption of interstitial fluid into the vascular compartment. Considerable quantities of fluid may be
drawn into the circulation during hemorrhage.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Reabsorption of Tissue Fluids (2 of 2)
Approximately 0.25 mL/min/kg of body weight (1 L/hr in the adult male) can be autotransfused from the interstitial spaces after acute blood loss.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Vasculature
Lined with smooth muscle. All vessels larger than capillaries
have layers of tissues (tunicae). Maintains blood flow by changes in
pressure and peripheral vascular resistance.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Vascular Pressure Gradients Fluid flows through a tube in
response to pressure gradients between the two ends of the tube.
It is not the absolute pressure in the tube that determines flow, but the difference in pressure between the two ends.
In humans, the two ends are the aorta and the vena cava.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Vasculature
Measurements of pressure in the vascular system: Systemic pressure
(left‑sided pressure) and Pulmonic pressure
(right‑sided pressure) Systemic pressure, like pulmonic
pressure, has two phases: systolic and diastolic.
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Diastolic Blood Pressure
Diastolic blood pressure is a reflection of peripheral vascular resistance. Pulse pressure is the difference between
these two pressures. Pressure is greatest at its origin (the
heart) and least at its terminating point (the venae cavae).
This pressure gradient changes significantly at the arteriole because of peripheral vascular resistance.
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Peripheral Vascular Resistance (Afterload) The total resistance against which
blood must be pumped. It is essentially a measure of friction
between the vessel walls and fluid, and between the molecules within the fluid itself (viscosity). Both oppose flow.
When resistance to flow increases, blood pressure must increase for the flow to remain constant.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Starling’s Law of the Heart 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.
The more blood the heart receives the more it pumps…
Increased end diastolic volume increases contractility.
Increases stroke volume. Increases cardiac output.
Starling curves at any end-diastolic volume. Increased sympathetic input increases stroke
volume. Decreased sympathetic input decreases stroke
volume.
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Resistance to Blood Flow Increases with… Increased fluid viscosity Increased vessel length Decreased vessel diameter
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Viscosity
The physical property of a liquid characterized by the friction between its component molecules (e.g., between the blood cells and between the plasma proteins)
Normally plays a minor role in blood flow regulation as it remains constant in healthy people
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Blood Flow Resistance (1 of 2)
Arteries are large and offer little resistance to flow unless they have an abnormal narrowing (stenosis).
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Blood Flow Resistance (2 of 2)
Arterioles have a much smaller diameter and offer the major resistance to blood flow. Smooth muscles in the arteriole walls
can relax or contract. Can change the diameter of the vessel
as much as fivefold. Arterial blood pressure is regulated
primarily by the vasoconstriction or vasodilation of these vessels.
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Microcirculation (1 of 3)
Can be divided into pulmonary microcirculation and peripheral microcirculation.
Pressure in each division is produced by the right and left heart, respectively.
Approximately 5% of the total circulating blood flow is always flowing through capillaries.
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Microcirculation (2 of 3)
Venules and veins serve as collecting channels and storage vessels (capacitance).
Normally contain 70% of the blood volume.
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Microcirculation (3 of 3)
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Mechanisms That Control Blood Flow Local control of blood flow by the
tissues Nervous control of blood flow
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Local Control
Blood usually flows through capillaries intermittently due to: The pulsatile manner of blood flow
resulting from cardiac pumping action and vasomotion
The intermittent constriction and dilation of arterioles and precapillary sphincters
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Vasomotion (1 of 3)
Regulated primarily by the concentration of oxygen in the tissues.
When oxygen concentration is low, the cells lining and adjacent to the closed capillaries secrete histamine, which is thought to be responsible for arteriolar smooth muscle vasodilation, causing the capillary to open.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Vasomotion (2 of 3)
Histamine is quickly destroyed in the blood and does not enter the general circulation.
As cells become reoxygenated they stop the histamine secretion, and the capillary closes.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Vasomotion (3 of 3)
A decrease in oxygen concentration leads to a local release of vasodilating substances, which allows blood flow to increase. This in turn increases the delivery of
oxygen and restores aerobic metabolism.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Nervous control of circulation is
accomplished by negative feedback
mechanisms.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
CNS Ischemia Response
CNS ischemia response is activated when blood flow to the vasomotor center of the medulla is decreased. In the presence of ischemia, the neurons
within the medulla stimulate the sympathetic nervous system.
Sympathetic vasoconstriction can elevate arterial pressure for as long as 10 minutes.
The cerebral ischemia response functions only in emergency situations.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Blood and Blood Components
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Blood
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.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Blood Components (1 of 2)
Erythrocyte: 45% Hemoglobin Hematocrit
Miscellaneous blood products: <1% Platelets Leukocytes
Monocytes, basophils, esonophils, neutrophils
Plasma: 54%
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Blood Components (2 of 2)
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Plasma (1 of 2)
Approximately 92% water The liquid portion of blood
Circulates salts, minerals, sugars, fats, and proteins throughout the body
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Plasma (2 of 2)
Contains 3 major proteins: Albumin
Most plentiful plasma protein Similar in consistency to egg whites Gives blood its gummy texture Helps keep water concentration of blood low
enough to allow water to diffuse readily from tissues into blood
Globulins serve 2 main functions: Alpha and beta globulins transport other proteins Gamma globulins give people immunity to disease
Fibrinogen Aids in blood clotting by forming a web of protein
fibers that binds blood cells together
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Other Functions of Plasma
Proteins function as an acid or base to correct changes in blood acidity.
Can temporarily meet nutritional need of the body should the body run short of food.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Proteins
Account for 50% of the body’s organic material Components of most body structures Roles in the chemical reactions in the body
Specialized proteins are responsible for: Immune responses Coagulation Digestion of foodstuffs Metabolism of nutrients Many other functions
Erythrocytes (RBCs)
Transport 99% of blood oxygen. Remaining 1% carried in plasma
Make up approximately 45% of the blood and are the most abundant cells in the body.
Provide oxygen to tissues and remove carbon dioxide.
Each RBC contains approximately 270 million hemoglobin molecules. Allow RBCs to pick up oxygen in the lungs and
release it to body tissuesBledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma
© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Leukocytes (WBCs)
Defend the body against various pathogens (bacteria, viruses, fungi, and parasites)
Produced in bone marrow and lymph glands Release reserves when pathogens
invade the body
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
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)
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Clotting (1 of 2)
Three-Step Process Vascular phase
Vasoconstriction Platelet phase
Tunica intima damaged Turbulent blood flow Frictional damage to platelets
Agglutination and aggregation Coagulation
Release of enzymes Extrinsic – nearby tissue Intrinsic – damaged platelets Fibrin release
Normal coagulation in 7–10 minutesBledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma
© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Clotting (2 of 2)
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Factors Affecting Clotting (1 of 2)
Movement of the wound site Aggressive fluid therapy
Increased BP and displaced clots Dilution of clotting factors
Low body temperature Ineffective clot formation
Medications ASA, heparin, Ticlid, warfarin (Coumadin)
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Factors Affecting Clotting (2 of 2)
Nature of the wound Transverse (clean tear)
Vessels constrict and draw inward Reduction of the lumen Reduction of blood loss
Longitudinal (crush injury) Constriction of the smooth
muscle Enlarges the wound Increases blood loss
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Stages of ShockCellular Level
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Four Stages
Stage 1: Vasoconstriction Stage 2: Capillary and venule
opening Stage 3: Disseminated intravascular
coagulation Stage 4: Multiple organ failure
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Stage 1: Vasoconstriction (1 of 4)
Vasoconstriction begins as minimal perfusion to capillaries continues. Oxygen and substrate delivery to the
cells supplied by these capillaries decreases.
Anaerobic metabolism replaces aerobic metabolism.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Stage 1: Vasoconstriction (2 of 4)
Production of lactate and hydrogen ions increases. The lining of the capillaries may begin to
lose the ability to retain large molecular structures within its walls.
Protein-containing fluid leaks into the interstitial spaces (leaky capillary syndrome).
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Stage 1: Vasoconstriction (3 of 4)
Sympathetic stimulation produces: Pale, sweaty skin Rapid, thready pulse Elevated blood glucose levels
The release of epinephrine dilates coronary, cerebral, and skeletal muscle arterioles and constricts other arterioles. Blood is shunted to the heart, brain, skeletal
muscle, and capillary flow to the kidneys and abdominal viscera decreases.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
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.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Stage 2: Capillary and Venule Opening (1 of 5)
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.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Stage 2: Capillary and Venule Opening (2 of 5)
As the syndrome continues, the precapillary sphincters relax with some expansion of the vascular space.
Postcapillary sphincters resist local effects and remain closed, causing blood to pool or stagnate in the capillary system, producing capillary engorgement.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Stage 2: Capillary and Venule Opening (3 of 5)
As increasing hypoxemia and acidosis lead to opening of additional venules and capillaries, the vascular space expands greatly. Even normal blood volume may be
inadequate to fill the container. The capillary and venule capacity may
become great enough to reduce the volume of available blood for the great veins and vena cava. Resulting in decreased venous return and a
fall in cardiac output.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Stage 2: Capillary and Venule Opening (4 of 5)
Low arterial blood pressure and many open capillaries result in stagnant capillary flow.
Sluggish blood flow and the reduced delivery of oxygen result in increased anaerobic metabolism and the production of lactic acid. The respiratory system attempts to
compensate for the acidosis by increasing ventilation to blow off carbon dioxide.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Stage 2: Capillary and Venule Opening (5 of 5)
As acidosis increases and pH falls, the RBCs may cluster together (rouleaux formation). Halts perfusion Affects nutritional flow and prevents removal of
cellular metabolites
Clotting mechanisms are also affected, leading to hypercoagulability.
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.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Stage 3: Disseminated Intravascular Coagulation (DIC) (1 of 4) Time of onset will depend on degree of
shock, patient age, and pre-existing medical conditions.
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.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Stage 3: Disseminated Intravascular Coagulation (DIC) (2 of 4) Stage 3 is resistant to treatment
(refractory shock), but is still reversible.
Blood begins to coagulate in the microcirculation, clogging capillaries. Capillaries become occluded by clumps of
RBCs. Decreases capillary perfusion and prevents
removal of metabolites Distal tissue cells use anaerobic
metabolism, and lactic acid production increases.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Stage 3: Disseminated Intravascular Coagulation (DIC) (3 of 4)
Lactic acid accumulates around the cell. Cell membranes no longer have the
energy needed to maintain homeostasis.
Water and sodium leak in, potassium leaks out, and the cells swell and die.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Stage 3: Disseminated Intravascular Coagulation (DIC) (4 of 4)
Pulmonary capillaries become permeable, leading to pulmonary edema. Decreases the absorption of oxygen and
results in possible alterations in carbon dioxide elimination
May lead to acute respiratory failure or adult respiratory distress syndrome (ARDS)
If shock and disseminated intravascular coagulation (DIC) continue, the patient progresses to multiple organ failure.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Stage 4: Multiple Organ Failure (1 of 2)
The amount of cellular necrosis required to produce organ failure varies with each organ and the underlying condition of the organ. Usually hepatic failure occurs, followed by renal
failure, and then heart failure. If capillary occlusion persists for more than 1 to 2
hours, the cells nourished by that capillary undergo changes that rapidly become irreversible.
In this stage, blood pressure falls dramatically (to levels of 60 mmHg or less). Cells can no longer use oxygen, and metabolism
stops.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Stage 4: Multiple Organ Failure (2 of 2)
If a critical amount of the vital organ is damaged by cellular necrosis, the organ soon fails. Failure of the liver is common and often presents
early. Capillary blockage may cause heart failure. GI bleeding and sepsis may result from GI mucosal
necrosis. Pancreatic necrosis may lead to further clotting
disorders and severe pancreatitis. Pulmonary thrombosis may produce
hemorrhage and fluid loss into the alveoli. Leading to death from respiratory failure.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Stages of ShockCellular Level
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Four Stages
Stage 1: Vasoconstriction Stage 2: Capillary and venule
opening Stage 3: Disseminated intravascular
coagulation Stage 4: Multiple organ failure
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Stage 1: Vasoconstriction (1 of 4)
Vasoconstriction begins as minimal perfusion to capillaries continues. Oxygen and substrate delivery to the
cells supplied by these capillaries decreases.
Anaerobic metabolism replaces aerobic metabolism.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Stage 1: Vasoconstriction (2 of 4)
Production of lactate and hydrogen ions increases. The lining of the capillaries may begin to
lose the ability to retain large molecular structures within its walls.
Protein-containing fluid leaks into the interstitial spaces (leaky capillary syndrome).
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Stage 1: Vasoconstriction (3 of 4)
Sympathetic stimulation produces: Pale, sweaty skin Rapid, thready pulse Elevated blood glucose levels
The release of epinephrine dilates coronary, cerebral, and skeletal muscle arterioles and constricts other arterioles. Blood is shunted to the heart, brain, skeletal
muscle, and capillary flow to the kidneys and abdominal viscera decreases.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
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.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Stage 2: Capillary and Venule Opening (1 of 5)
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.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Stage 2: Capillary and Venule Opening (2 of 5)
As the syndrome continues, the precapillary sphincters relax with some expansion of the vascular space.
Postcapillary sphincters resist local effects and remain closed, causing blood to pool or stagnate in the capillary system, producing capillary engorgement.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Stage 2: Capillary and Venule Opening (3 of 5)
As increasing hypoxemia and acidosis lead to opening of additional venules and capillaries, the vascular space expands greatly. Even normal blood volume may be
inadequate to fill the container. The capillary and venule capacity may
become great enough to reduce the volume of available blood for the great veins and vena cava. Resulting in decreased venous return and a
fall in cardiac output.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Stage 2: Capillary and Venule Opening (4 of 5)
Low arterial blood pressure and many open capillaries result in stagnant capillary flow.
Sluggish blood flow and the reduced delivery of oxygen result in increased anaerobic metabolism and the production of lactic acid. The respiratory system attempts to
compensate for the acidosis by increasing ventilation to blow off carbon dioxide.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Stage 2: Capillary and Venule Opening (5 of 5)
As acidosis increases and pH falls, the RBCs may cluster together (rouleaux formation). Halts perfusion Affects nutritional flow and prevents removal of
cellular metabolites
Clotting mechanisms are also affected, leading to hypercoagulability.
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.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Stage 3: Disseminated Intravascular Coagulation (DIC) (1 of 4) Time of onset will depend on degree of
shock, patient age, and pre-existing medical conditions.
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.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Stage 3: Disseminated Intravascular Coagulation (DIC) (2 of 4) Stage 3 is resistant to treatment
(refractory shock), but is still reversible.
Blood begins to coagulate in the microcirculation, clogging capillaries. Capillaries become occluded by clumps of
RBCs. Decreases capillary perfusion and prevents
removal of metabolites Distal tissue cells use anaerobic
metabolism, and lactic acid production increases.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Stage 3: Disseminated Intravascular Coagulation (DIC) (3 of 4)
Lactic acid accumulates around the cell. Cell membranes no longer have the
energy needed to maintain homeostasis.
Water and sodium leak in, potassium leaks out, and the cells swell and die.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Stage 3: Disseminated Intravascular Coagulation (DIC) (4 of 4)
Pulmonary capillaries become permeable, leading to pulmonary edema. Decreases the absorption of oxygen and
results in possible alterations in carbon dioxide elimination
May lead to acute respiratory failure or adult respiratory distress syndrome (ARDS)
If shock and disseminated intravascular coagulation (DIC) continue, the patient progresses to multiple organ failure.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Stage 4: Multiple Organ Failure (1 of 2)
The amount of cellular necrosis required to produce organ failure varies with each organ and the underlying condition of the organ. Usually hepatic failure occurs, followed by renal
failure, and then heart failure. If capillary occlusion persists for more than 1 to 2
hours, the cells nourished by that capillary undergo changes that rapidly become irreversible.
In this stage, blood pressure falls dramatically (to levels of 60 mmHg or less). Cells can no longer use oxygen, and metabolism
stops.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Stage 4: Multiple Organ Failure (2 of 2)
If a critical amount of the vital organ is damaged by cellular necrosis, the organ soon fails. Failure of the liver is common and often presents
early. Capillary blockage may cause heart failure. GI bleeding and sepsis may result from GI mucosal
necrosis. Pancreatic necrosis may lead to further clotting
disorders and severe pancreatitis. Pulmonary thrombosis may produce
hemorrhage and fluid loss into the alveoli. Leading to death from respiratory failure.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Stages of ShockCellular Level
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Four Stages
Stage 1: Vasoconstriction Stage 2: Capillary and venule
opening Stage 3: Disseminated intravascular
coagulation Stage 4: Multiple organ failure
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Stage 1: Vasoconstriction (1 of 4)
Vasoconstriction begins as minimal perfusion to capillaries continues. Oxygen and substrate delivery to the
cells supplied by these capillaries decreases.
Anaerobic metabolism replaces aerobic metabolism.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Stage 1: Vasoconstriction (2 of 4)
Production of lactate and hydrogen ions increases. The lining of the capillaries may begin to
lose the ability to retain large molecular structures within its walls.
Protein-containing fluid leaks into the interstitial spaces (leaky capillary syndrome).
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Stage 1: Vasoconstriction (3 of 4)
Sympathetic stimulation produces: Pale, sweaty skin Rapid, thready pulse Elevated blood glucose levels
The release of epinephrine dilates coronary, cerebral, and skeletal muscle arterioles and constricts other arterioles. Blood is shunted to the heart, brain, skeletal
muscle, and capillary flow to the kidneys and abdominal viscera decreases.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
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.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Stage 2: Capillary and Venule Opening (1 of 5)
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.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Stage 2: Capillary and Venule Opening (2 of 5)
As the syndrome continues, the precapillary sphincters relax with some expansion of the vascular space.
Postcapillary sphincters resist local effects and remain closed, causing blood to pool or stagnate in the capillary system, producing capillary engorgement.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Stage 2: Capillary and Venule Opening (3 of 5)
As increasing hypoxemia and acidosis lead to opening of additional venules and capillaries, the vascular space expands greatly. Even normal blood volume may be
inadequate to fill the container. The capillary and venule capacity may
become great enough to reduce the volume of available blood for the great veins and vena cava. Resulting in decreased venous return and a
fall in cardiac output.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Stage 2: Capillary and Venule Opening (4 of 5)
Low arterial blood pressure and many open capillaries result in stagnant capillary flow.
Sluggish blood flow and the reduced delivery of oxygen result in increased anaerobic metabolism and the production of lactic acid. The respiratory system attempts to
compensate for the acidosis by increasing ventilation to blow off carbon dioxide.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Stage 2: Capillary and Venule Opening (5 of 5)
As acidosis increases and pH falls, the RBCs may cluster together (rouleaux formation). Halts perfusion Affects nutritional flow and prevents removal of
cellular metabolites
Clotting mechanisms are also affected, leading to hypercoagulability.
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.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Stage 3: Disseminated Intravascular Coagulation (DIC) (1 of 4) Time of onset will depend on degree of
shock, patient age, and pre-existing medical conditions.
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.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Stage 3: Disseminated Intravascular Coagulation (DIC) (2 of 4) Stage 3 is resistant to treatment
(refractory shock), but is still reversible.
Blood begins to coagulate in the microcirculation, clogging capillaries. Capillaries become occluded by clumps of
RBCs. Decreases capillary perfusion and prevents
removal of metabolites Distal tissue cells use anaerobic
metabolism, and lactic acid production increases.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Stage 3: Disseminated Intravascular Coagulation (DIC) (3 of 4)
Lactic acid accumulates around the cell. Cell membranes no longer have the
energy needed to maintain homeostasis.
Water and sodium leak in, potassium leaks out, and the cells swell and die.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Stage 3: Disseminated Intravascular Coagulation (DIC) (4 of 4)
Pulmonary capillaries become permeable, leading to pulmonary edema. Decreases the absorption of oxygen and
results in possible alterations in carbon dioxide elimination
May lead to acute respiratory failure or adult respiratory distress syndrome (ARDS)
If shock and disseminated intravascular coagulation (DIC) continue, the patient progresses to multiple organ failure.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Stage 4: Multiple Organ Failure (1 of 2)
The amount of cellular necrosis required to produce organ failure varies with each organ and the underlying condition of the organ. Usually hepatic failure occurs, followed by renal
failure, and then heart failure. If capillary occlusion persists for more than 1 to 2
hours, the cells nourished by that capillary undergo changes that rapidly become irreversible.
In this stage, blood pressure falls dramatically (to levels of 60 mmHg or less). Cells can no longer use oxygen, and metabolism
stops.
Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Stage 4: Multiple Organ Failure (2 of 2)
If a critical amount of the vital organ is damaged by cellular necrosis, the organ soon fails. Failure of the liver is common and often presents
early. Capillary blockage may cause heart failure. GI bleeding and sepsis may result from GI mucosal
necrosis. Pancreatic necrosis may lead to further clotting
disorders and severe pancreatitis. Pulmonary thrombosis may produce
hemorrhage and fluid loss into the alveoli. Leading to death from respiratory failure.