Shock and Hemorrhage

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



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



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



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.


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.

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.


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.


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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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



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



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




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 PNS and SNS always act in balance Baroreceptors: monitor BP Chemoreceptors Hormone regulation Reabsorption of tissue fluids


Cardiovascular System Regulation (2 of 3)

Parasympathetic Nervous System Decrease

Heart rate Strength of contractions Blood pressure

Increase Digestive system Kidneys


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


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.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.


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

Action Increase in peripheral vascular resistance Increase water retention by kidneys Decrease urine output Splenic vasoconstriction

200 mL of free blood to circulation



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



Aldosterone Release

Adrenal cortex Stimulated by angiotensin II

Action Maintain kidney ion balance Retention of sodium and water Reduce insensible fluid loss



Glucagon Release

Alpha cells of pancreas Triggered by epinephrine

Action Causes liver and skeletal muscles to

convert glycogen into glucose Gluconeogenesis



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


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.


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.


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


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 tissuesBledsoe et al., Paramedic Care Principles & Practice Volume 4:Trauma


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 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



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 lumen Reduction of blood loss

Longitudinal (crush injury) Constriction of the smooth

muscle Enlarges the wound Increases blood loss




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Shock and Hemorrhage