Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma © 2006 by Pearson Education, Inc. Upper Saddle River, NJ Chapter 4 Hemorrhage and

Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma© 2006 by Pearson Education, Inc. Upper Saddle River, NJ

Chapter 4 Hemorrhage and Shock


Introduction to Hemorrhage and Shock

Hemorrhage

Shock

Topics



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 systemSlows rate

Mediated by vagus nerve

Sympathetic nervous systemIncreases rate

Cardiac plexus



Key TermsStroke VolumePreloadVentricular FillingStarling’s Law of the heartAfterload (End Diastolic Pressure or EDP)Cardiac Output– SV x HR– 5 liters/minute

Fick Principle


Arteries– Tunica Adventitia– Tunica Media– Tunica Intima

ArterioleCapillary: 7% of total blood volumeVenuleVein– Constriction returns 20% (1 liter) of blood to

active circulation

} 64% of blood volume

} 13% of blood volume





Cardiac Physiology

Vena Cavaand

SystemicVeins

Aortaand

SystemicArteries

SystemicCapillaries

PulmonaryArteries

LUNGS

PulmonaryVeins

RightAtrium

RightVentricle

LeftAtrium

LeftVentricle


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.


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).


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


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


Cardiovascular System Regulation (1 of 3)

PNS and SNS always act in balance

Baroreceptors: monitor BP

Chemoreceptors

Hormone regulation

Reabsorption of tissue fluids



Parasympathetic Nervous System

Decrease – Heart rate– Strength of contractions– Blood pressure

Increase– Digestive system– Kidneys



Sympathetic Nervous SystemIncrease– Body activity– Heart rate– Strength of contractions– Vascular constriction

Bowel and digestive visceraDecreased urine production

– Respirations– Bronchodilation

Increases skeletal muscle perfusion


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.



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



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.



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.



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.


The vasoconstriction in peripheral vascular beds results in the

characteristic pale, cold skin of patients suffering from hypovolemic shock.


Chemoreceptor Reflexes

Chemoreceptors– Monitor level of CO2 in CSF

– Monitor level of O2 in blood


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.


CV System and Hormone Regulation (1 of 7)

Catecholamines– Epinephrine– Norepinephrine– Actions

Alpha 1

Alpha 2

Beta 1

Beta 2



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



Antidiuretic Hormone (ADH)– AKA: Arginine Vasopressin (AVP)– Released

Posterior pituitary

Drop in BP or increase in serum osmolarity

– ActionIncrease in peripheral vascular resistance

Increase water retention by kidneys

Decrease urine output

Splenic vasoconstriction200 mL of free blood to circulation



Angiotensin II– Released

Primary chemical from kidneys

Lowered BP and decreased perfusion

– ActionConverted 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



Aldosterone– Release

Adrenal cortex

Stimulated by angiotensin II

– ActionMaintain kidney ion balance

Retention of sodium and water

Reduce insensible fluid loss



Glucagon– Release

Alpha cells of pancreas

Triggered by epinephrine

– ActionCauses liver and skeletal muscles to convert glycogen into glucose

Gluconeogenesis



Insulin– Release

Beta cells of pancreas

– ActionFacilitates transport of glucose across cell membrane

Erythropoietin– Release

Kidneys

Hypoperfusion or hypoxia

– ActionIncreases production and maturation of RBCs in the bone marrow


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.


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.


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.


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.


VasculatureMeasurements 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.


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.


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.


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


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


Blood Flow Resistance (1 of 2)

Arteries are large and offer little resistance to flow unless they have an abnormal narrowing (stenosis).


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.


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.



Venules and veins serve as collecting channels and storage vessels (capacitance).

Normally contain 70% of the blood volume.




Mechanisms That Control Blood Flow

Local control of blood flow by the tissues

Nervous control of blood flow


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


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.


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.


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.


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


Contains 3 major proteins: – Albumin

Most plentiful plasma proteinSimilar in consistency to egg whitesGives blood its gummy textureHelps 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 proteinsGamma globulins give people immunity to disease

– FibrinogenAids in blood clotting by forming a web of protein fibers that binds blood cells together

Plasma (2 of 2)


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


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)


Clotting (1 of 2)

Three-Step Process– Vascular phase

Vasoconstriction

– Platelet phaseTunica intima damaged

Turbulent blood flowFrictional damage to platelets

Agglutination and aggregation

– CoagulationRelease of enzymes

Extrinsic – nearby tissueIntrinsic – damaged plateletsFibrin release

Normal coagulation in 7–10 minutes


Clotting (2 of 2)


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)


Factors Affecting Clotting (2 of 2)

Nature of the wound– Transverse (clean tear)

Vessels constrict and draw inward

Reduction of the lumenReduction of blood loss

– Longitudinal (crush injury)Constriction of the smooth muscle

Enlarges the woundIncreases blood loss


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.



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).



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.



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.



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.



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.



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.



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.



(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.



(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.



(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 pressureElevationIcePressure pointsConstricting bandTourniquet

May use a BP cuff by inflating the cuff 20–30 mmHg above the SBPRelease 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 BleedCauses: 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

men5 L (10 units)

– 6.5% CBV in women4.6 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

EpinephrineNorepinephrine

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



Decreased pulse strength

Narrowing pulse pressure

Significant catecholamine release– Increase PVR– Cool, clammy skin and thirst– Increased anxiety and agitation– Normal renal output



25–35% loss of CBV– 1250–1750 mL

Late decompensation (early irreversible)– Compensatory mechanisms unable to

cope with loss of blood volume



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

– AthletesGreater fluid and cardiac capacity

– ObeseCBV 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 AGGRESIVELY!

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 IllnessShould 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



Initial Assessment– General Impression

Obvious Bleeding

– Mental Status– CABC– Interventions

Manage as you goO2

Bleeding controlShockBLS before ALS!



Focused H&P– Rapid Trauma Assessment

Full head to toe

Consider air medical if stage 2+ blood loss

– Focused Physical ExamGuided by c/c

– Vitals, SAMPLE, and OPQRST– Additional Assessment

Orthostatic hypotension

Tilt test: 20BP or P from supine to sitting



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



Ongoing Assessment– Reassess vitals and mental status:

Q 5 min: UNSTABLE patientsQ 15 min: STABLE patients

– Reassess interventions:OxygenETIVMedication actions

– Trending: improvement vs. deteriorationPulse 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

– ManagementGentle direct pressure

Fluid drainage from ears and nose

DO NOT pack

Cover and bandage loosely

Neck Wounds– Presentation

Large vessel can entrap air

– ManagementConsider direct digital pressure

Occlusive dressing


Specific Wound Considerations (2 of 2)

Gaping Wounds– Presentation

Multiple sitesGaping prevents uniform pressure

– ManagementBulky dressing

Trauma dressing

Sterile, non-adherent surface to woundCompression dressing

Crush Injury– Presentation

Difficult to locate source of bleedingNormal hemorrhage control mechanism non-functional

– ManagementConsider an air-splint and pressure dressingConsider 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 ControlFluid 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 PVRReduce vascular volumeIncrease central CBVImmobilize lower extremities

– AssessPulmonary edemaPregnancyVital signs


Summary


Hemorrhage

Shock

Documents

Bledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma © 2006 by Pearson Education, Inc. Upper Saddle River, NJ Chapter 4 Hemorrhage and