HEMORRHAGE AND SHOCK

TOPICS

• Introduction to Hemorrhage and Shock

• Hemorrhage

• Shock

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

HEMORRHAGE

• Circulatory System

• Hemorrhage Classification

• Clotting

• Factors Affecting Clotting

• Hemorrhage Control

• Stages of Hemorrhage

• Hemorrhage Assessment

• Hemorrhage Management

CARDIAC ANATOMY

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

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)

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

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

CIRCULATORY SYSTEM (4 OF 4)

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.

THE VASOCONSTRICTION IN PERIPHERAL VASCULAR BDS

RESULTS IN THE CHARACTERISTIC PALE, COLD SKIN OF PATIENTS SUFFERING FROM HYPOVOLEMIC SHOCK.

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.

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.

RESISTANCE TO BLOOD FLOW INCREASES WITH…

• Increased fluid viscosity

• Increased vessel length

• Decreased vessel diameter

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.

Nervous control of circulation is

accomplished by negative feedback

mechanisms.

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.

BLOOD AND BLOOD COMPONENTS

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.

BLOOD COMPONENTS (1 OF 2)

• Erythrocyte: 45%

• Hemoglobin

• Hematocrit

• Miscellaneous blood products: <1%

• Platelets

• Leukocytes

• Monocytes, basophils, esonophils, neutrophils

• Plasma: 54%

Blood Components (2 of 2)

PLASMA (1 OF 2)

• Approximately 92% water

• The liquid portion of blood

• Circulates salts, minerals, sugars, fats, and proteins throughout the body

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

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.

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 tissues

Bledsoe et al., Essentials of Paramedic Care: Division 1II© 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

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)

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.

SHOCK AND HEMORRHAGE

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

• Results from soft tissue injury.

• Accounts for nearly 10 million emergency department visits in the United States each year.

• Most soft tissue trauma is accompanied by mild hemorrhage and is not life threatening.

• Can carry significant risks of patient morbidity and disfigurement

• The seriousness of the injury is dependent on:• Anatomical source of the hemorrhage (arterial, venous,

capillary)• Degree of vascular disruption• Amount of blood loss that can be tolerated by the patient

INTERNAL HEMORRHAGE (1 OF 2)

• 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

INTERNAL HEMORRHAGE (2 OF 2)

• Signs and symptoms that may suggest significant internal hemorrhage include:

• Bright red blood from mouth, rectum, or other orifice

• Coffee-ground appearance of vomitus

• Melena (black, tarry stools)

• Dizziness or syncope on sitting or standing

• Orthostatic hypotension

Internal hemorrhage is associated with higher morbidity and mortality

than external hemorrhage.

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

FICK PRINCIPLE

• A method for measuring cardiac output.• 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.

• 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.

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

STAGES OF HEMORRHAGE STAGE 2 (1 OF 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

• Increase PVR

• Cool, clammy skin and thirst

• Increased anxiety and agitation

• Normal renal output

STAGES OF HEMORRHAGE STAGE 3 (1 OF 2)

• 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 (2 OF 2)

• Classic Shock

• Weak, thready, rapid pulse

• Narrowing pulse pressure

• Tachypnea

• Anxiety, restlessness

• Decreased LOC and AMS

• Pale, cool, and clammy skin

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

STAGES OF HEMORRHAGE CONCOMITANT FACTORS (1 OF 2)

• 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)

STAGES OF HEMORRHAGE CONCOMITANT FACTORS (2 OF 2)

• Children

• CBV 8–9% of body weight

• Poor compensatory mechanisms

• TREAT AGGRESSIVELY!

• Elderly

• Decreased CBV

• Medications

• BP

• Anticoagulants

HEMORRHAGE ASSESSMENT (1 OF 5)

• Scene Size-up• Is it safe?

• BSI– Blood loss

• Law enforcement

• Mechanism of Injury/Nature of Illness• Should only be used in conjunction with vital signs and other

clinical signs of injury to determine the probability of injury

• Number of Patients• Need for Additional Resources

HEMORRHAGE ASSESSMENT (2 OF 5)

• Initial Assessment• General Impression

• Obvious bleeding

• Mental Status• CABC• Interventions

• Manage as you go• O2

• Bleeding control• Shock• BLS before ALS!

HEMORRHAGE ASSESSMENT (3 OF 5)

• Focused H&P• Rapid Trauma Assessment

• Full head to toe

• Consider air medical if stage 2+ blood loss

• Focused Physical Exam• Guided by c/c

• Vitals, SAMPLE, and OPQRST

• Additional Assessment• Orthostatic hypotension

• Tilt test: 20

• BP or P from supine to sitting

HEMORRHAGE ASSESSMENT (4 OF 5)

FRACTURES AND BLOOD LOSS

• Pelvic fracture:

• Femur fracture:

• Tibia/fibula fracture:

• Hematomas and contusions:

2,000 mL

1,500 mL

500–750 mL

500 mL

HEMORRHAGE ASSESSMENT (5 OF 5)

• 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 TISSUE

PERFUSION.

SHOCK MANAGEMENT

SPECIFIC WOUND CONSIDERATIONS

(1 OF 2)

• 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 nonfunctional

• Management• Consider an air-

splint and pressure dressing

• Consider tourniquet

TRANSPORT CONSIDERATIONS

• Consider rapid transport:

• 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

SUMMARY

• Introduction to Hemorrhage and Shock

• Hemorrhage

• Shock