Shock and Hemorrhage

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Transcript Shock and Hemorrhage

Chapter 4 Hemorrhage and Shock

Bledsoe et al.,

Paramedic Care Principles & Practice Volume 4:Trauma

Topics

Introduction to Hemorrhage and Shock Hemorrhage Shock Bledsoe et al.,

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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.,

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Hemorrhage

Circulatory System Hemorrhage Classification Clotting Factors Affecting Clotting Hemorrhage Control Stages of Hemorrhage Hemorrhage Assessment Hemorrhage Management Bledsoe et al.,

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Cardiac Anatomy

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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.,

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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.,

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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 Bledsoe et al.,

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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.,

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Circulatory System

(3 of 4) Arteries – Tunica Adventitia – Tunica Media – Tunica Intima Arteriole } 13% of blood volume Capillary: 7% of total blood volume Venule } 64% of blood volume Vein – Constriction returns 20% (1 liter) of blood to active circulation Bledsoe et al.,

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Circulatory System

(4 of 4) Bledsoe et al.,

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Cardiac Physiology

Systemic Capillaries Vena Cava and Systemic Veins Aorta and Systemic Arteries Right Atrium Left Ventricle Right Ventricle

Left

Atrium Pulmonary Arteries Pulmonary Veins

LUNGS

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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 Bledsoe et al.,

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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 O 2 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.,

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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 Bledsoe et al.,

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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 Bledsoe et al.,

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Cardiovascular System Regulation

(1 of 3) PNS and SNS always act in balance Baroreceptors: monitor BP Chemoreceptors Hormone regulation Reabsorption of tissue fluids Bledsoe et al.,

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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 Bledsoe et al.,

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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 Bledsoe et al.,

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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.,

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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.

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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.

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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.

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The vasoconstriction in peripheral vascular beds results in the characteristic pale, cold skin of patients suffering from hypovolemic shock.

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Chemoreceptor Reflexes

Chemoreceptors – Monitor level of CO 2 – Monitor level of O 2 in CSF in blood Bledsoe et al.,

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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.

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CV System and Hormone Regulation

(1 of 7) Catecholamines – Epinephrine – Norepinephrine – Actions Alpha 1 Alpha 2 Beta 1 Beta 2 Bledsoe et al.,

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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 Bledsoe et al.,

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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.,

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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 Bledsoe et al.,

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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 Bledsoe et al.,

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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 Bledsoe et al.,

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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 Bledsoe et al.,

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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.,

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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.

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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.

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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.

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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.

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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 Bledsoe et al.,

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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 Bledsoe et al.,

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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) Bledsoe et al.,

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Mechanisms That Control Blood Flow

Local control of blood flow by the tissues Nervous control of blood flow Bledsoe et al.,

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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.,

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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.

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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.

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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.

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Nervous control of circulation is accomplished by negative feedback mechanisms.

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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.

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Blood and Blood Components

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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.

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Blood Components

(1 of 2) Erythrocyte: 45% – Hemoglobin – Hematocrit Miscellaneous blood products: <1% – Platelets – Leukocytes Monocytes, basophils, esonophils, neutrophils Plasma: 54% Bledsoe et al.,

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Blood Components

(2 of 2) Bledsoe et al.,

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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.,

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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.,

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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.

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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 Bledsoe et al.,

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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.,

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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.,

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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.,

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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 minutes Bledsoe et al.,

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Clotting

(2 of 2) Bledsoe et al.,

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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.,

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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.,

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Stages of Shock Cellular Level

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Four Stages

Stage 1: Vasoconstriction Stage 2: Capillary and venule opening Stage 3: Disseminated intravascular coagulation Stage 4: Multiple organ failure Bledsoe et al.,

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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.,

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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).

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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.

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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.

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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.,

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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.

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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.

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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.

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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.

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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.

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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.,

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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.

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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.,

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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.,

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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.

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Shock and Hemorrhage

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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 Bledsoe et al.,

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Defining Shock

(2 of 2) Shock is not adequately defined by: – Pulse rate – Blood pressure – Cardiac function – Hypovolemia – Loss of systemic vascular resistance Bledsoe et al.,

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Hemorrhage Classification

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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 Bledsoe et al.,

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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 Bledsoe et al.,

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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 Bledsoe et al.,

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Internal hemorrhage is associated with higher morbidity and mortality than external hemorrhage.

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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 Bledsoe et al.,

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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.

Bledsoe et al.,

Paramedic Care Principles & Practice Volume 4:Trauma

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 Bledsoe et al.,

Paramedic Care Principles & Practice Volume 4:Trauma

Tourniquets are ONLY used as a last resort!

Bledsoe et al.,

Paramedic Care Principles & Practice Volume 4:Trauma

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 Bledsoe et al.,

Paramedic Care Principles & Practice Volume 4:Trauma

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) Bledsoe et al.,

Paramedic Care Principles & Practice Volume 4:Trauma

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 Bledsoe et al.,

Paramedic Care Principles & Practice Volume 4:Trauma

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 Bledsoe et al.,

Paramedic Care Principles & Practice Volume 4:Trauma

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 Bledsoe et al.,

Paramedic Care Principles & Practice Volume 4:Trauma

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 Bledsoe et al.,

Paramedic Care Principles & Practice Volume 4:Trauma

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 Bledsoe et al.,

Paramedic Care Principles & Practice Volume 4:Trauma

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 Bledsoe et al.,

Paramedic Care Principles & Practice Volume 4:Trauma

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) Bledsoe et al.,

Paramedic Care Principles & Practice Volume 4:Trauma

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 Bledsoe et al.,

Paramedic Care Principles & Practice Volume 4:Trauma

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 Bledsoe et al.,

Paramedic Care Principles & Practice Volume 4:Trauma

Hemorrhage Assessment

(2 of 5) Initial Assessment – General Impression Obvious Bleeding – Mental Status – CABC – Interventions Manage as you go O 2 Bleeding control Shock BLS before ALS!

Bledsoe et al.,

Paramedic Care Principles & Practice Volume 4:Trauma

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 Bledsoe et al.,

Paramedic Care Principles & Practice Volume 4:Trauma

Hemorrhage Assessment

(4 of 5) Fractures and Blood Loss Pelvic fracture: Femur fracture: Tibia/fibula fracture: 2,000 mL 1,500 mL 500 –750 mL Bledsoe et al.,

Paramedic Care Principles & Practice Volume 4:Trauma

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 CO 2 levels Bledsoe et al.,

Paramedic Care Principles & Practice Volume 4:Trauma

SHOCK is… INADEQUATE TISSUE PERFUSION.

Bledsoe et al.,

Paramedic Care Principles & Practice Volume 4:Trauma

Shock Management

Bledsoe et al.,

Paramedic Care Principles & Practice Volume 4:Trauma

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 Bledsoe et al.,

Paramedic Care Principles & Practice Volume 4:Trauma

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 Bledsoe et al.,

Paramedic Care Principles & Practice Volume 4:Trauma

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 Bledsoe et al.,

Paramedic Care Principles & Practice Volume 4:Trauma

Shock Management

(1 of 2) Airway and Breathing – NRB – PPV (overdrive respiration) – ET – CPAP – PEEP Any injury to the head or torso is Hemorrhage Control ALSO considered an Fluid Resuscitation injury to the spine.

– 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. Bledsoe et al.,

Paramedic Care Principles & Practice Volume 4:Trauma

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 Bledsoe et al.,

Paramedic Care Principles & Practice Volume 4:Trauma

Summary

Introduction to Hemorrhage and Shock Hemorrhage Shock Bledsoe et al.,

Paramedic Care Principles & Practice Volume 4:Trauma