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Pathophysiology of Hemorrhage

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0 Chapter 18 Bleeding and Shock

1 Pathophysiology of Hemorrhage
Simply means bleeding Can range from a “nick,” to a severely spurting artery, to a ruptured spleen External bleeding (visible hemorrhage) Internal bleeding

2 External Hemorrhage (1 of 2)
External bleeding Usually due to a break in the skin Extent or severity Bleeding from a capillary Bleeding from a vein Bleeding from an artery

3 External Hemorrhage (2 of 2)
Injuries Do not always have serious hemorrhaging Other injuries may cause more bleeding than expected.

4 Internal Hemorrhage (1 of 3)
Internal bleeding As a result of trauma Nontraumatic Cases of GI bleeding from the upper or lower GI tract Ruptured ectopic pregnancies Ruptured aneurysms

5 Internal Hemorrhage (2 of 3)
Must be treated promptly Signs do not always develop quickly. Pay close attention to patient complaints of pain or tenderness, development of tachycardia, and pallor. Be alert for the development of shock.

6 Internal Hemorrhage (3 of 3)
Management Focuses on: Treatment of shock Minimizing movement of the injured or bleeding part or region Rapid transport Eventually will need a surgical procedure to stop the bleeding

7 Controlled Versus Uncontrolled Hemorrhage (1 of 3)
Serious emergency Search for life-threatening bleeding. If the hemorrhage cannot be controlled in the field Concentrate on attempting to control the bleeding as you rapidly transport the patient

8 Controlled Versus Uncontrolled Hemorrhage (2 of 3)
External bleeding Most can be managed with direct pressure Arterial bleeding may take 5 or more minutes of direct pressure to form a clot. Use of a tourniquet

9 Controlled Versus Uncontrolled Hemorrhage (3 of 3)
Internal bleeding Most cases are rarely fully controlled in the prehospital setting. Rapid transport Pneumatic antishock garment/military antishock trousers (PASG/MAST)

10 The Significance of Bleeding (1 of 5)
Blood loss Often difficult to determine Looks different on different surfaces Patient’s presentation and your assessment direct your care.

11 The Significance of Bleeding (2 of 5)
Averages Human adult male bodies contain approximately 70 mL/kg. Adult female bodies contain approximately 65 mL/kg. Body cannot tolerate an acute loss of more than 20% of this total blood volume.

12 The Significance of Bleeding (3 of 5)
Averages (continued) If a typical adult loses more than 1 L of blood: Significant changes in vital signs will occur. Increasing heart and respiratory rates Decreasing blood pressure Infants and children

13 The Significance of Bleeding (4 of 5)
Compensation Depends on the rate of bleeding Healthy adult can donate one unit of blood in a period of 15 to 20 minutes without having ill effects. If a similar blood loss occurs in a much shorter period, hypovolemic shock may rapidly develop.

14 The Significance of Bleeding (5 of 5)
Serious if any of the following conditions are present A significant MOI Poor general appearance of the patient Signs and symptoms of shock Significant amount of blood loss Rapid blood loss Uncontrollable bleeding

15 Physiologic Response to Hemorrhage (1 of 4)
Bleeding from an artery Bright red Spurts in time with the pulse Difficult to control Bleeding from an open vein Much darker Flows steadily Easier to manage

16 Physiologic Response to Hemorrhage (2 of 4)
Bleeding from damaged capillary vessels Dark red Oozes steadily but slowly Venous and capillary bleeding is more likely to clot spontaneously. On its own Bleeding tends to stop rather quickly. Response to internal clotting mechanisms and exposure to air

17 Physiologic Response to Hemorrhage (3 of 4)
Hemostasis When vessels are lacerated Open ends of the vessel begin to narrow. Platelets aggregate at the site. Bleeding will not stop if a clot does not form. Direct contact with body tissues and fluids or the external environment commonly triggers the blood’s clotting factors.

18 Physiologic Response to Hemorrhage (4 of 4)
Hemostatic system may fail Medications Severe injury Only part of the vessel wall is cut. Acute blood loss may result in death before vasoconstriction and clotting can help.

19 Assessment of a Bleeding Patient (1 of 5)
Scene size-up Begins assessment of any patient General impression and initial assessment once the scene is deemed safe to enter BSI Gloves Mask Eyeshield Gown

20 Assessment of a Bleeding Patient (2 of 5)
Initial assessment Determine the patient’s mental status. Locate and manage immediate life threats. Ensure that the patient has a patent airway. If the patient has minor external bleeding, note it and move on.

21 Assessment of a Bleeding Patient (3 of 5)
MOI Trauma patients May be best indicator of internal injury or bleeding

22 Assessment of a Bleeding Patient (4 of 5)
Focused history Elaborate on the patient’s chief complaint using the OPQRST mnemonic. Obtain a history of the present illness using SAMPLE. Look for signs of shock. Ask the patient about medications and about any history of clotting insufficiency.

23 Assessment of a Bleeding Patient (5 of 5)
Physical exam Note the color of bleeding. Try to determine its source. Coffee-ground emesis Melena Hematochezia Hematuria Nonmenstrual vaginal bleeding

24 Management of a Bleeding Patient (1 of 3)
Managing external hemorrhage Steps to control hemorrhaging Apply direct pressure over the wound. Elevate the injury above the level of the heart if no fracture is suspected. Apply a pressure dressing. Apply pressure at the appropriate pressure point while maintaining direct pressure. Tourniquet is generally a last resort.

25 Management of a Bleeding Patient (2 of 3)
Bleeding from the nose, ears, and mouth Epistaxis May indicate a skull fracture Applying pressure increases intracranial pressure. Cover the bleeding site loosely with sterile gauze pad. May contain cerebrospinal fluid

26 Management of a Bleeding Patient (3 of 3)
Bleeding from other areas Control bleeding through use of direct pressure and elevation. Apply pressure dressings. Use splints as necessary. Pack large, gaping wounds with sterile dressings. Keep the patient warm and in the appropriate position.

27 Special Management Techniques (1 of 3)
Fractures Most bleeding occurs because the sharp ends lacerate vessels, muscles, and other tissues. As long as the fracture remains unstable, the bone end will move and continue to damage tissues and vessels. Immobilizing is a priority in the prompt control of bleeding.

28 Special Management Techniques (2 of 3)
Air splints Can control the bleeding associated with severe soft-tissue injuries or fractures Stabilize fractures Act like a pressure dressing applied to an entire extremity rather than to a small, local area Monitor circulation Not appropriate for use on arterial bleeding

29 Special Management Techniques (3 of 3)
Hemostats May be helpful when a vessel has been severed Simply apply hemostats to the ends of the vessel. Tourniquets Use for partial or complete amputation or when other methods of bleeding control have proved ineffective. Can cause permanent damage

30 Managing Internal Hemorrhage (1 of 2)
Definitive management Occurs in the hospital Prehospital management Treating for shock and splinting injured extremities: Keep the patient supine. Open the airway. Check breathing and pulse.

31 Managing Internal Hemorrhage (2 of 2)
Prehospital management (continued) Administer high-flow supplemental oxygen. Assist ventilation if needed. Splint broken bones or joint injuries. Place blankets under and over the patient. Consider giving pain medication. Monitor the serial vital signs.

32 Transportation of Patients With Hemorrhage
In case of hemorrhage Not whether the patient will be transported How fast the decision should be made Where the patient should be taken

33 Pathophysiology of Shock (1 of 4)
Hypoperfusion Occurs when the level of tissue perfusion decreases below normal Early decreased tissue perfusion may result in subtle changes long before a patient’s vital signs appear abnormal.

34 Pathophysiology of Shock (2 of 4)
State of collapse and failure of the cardiovascular system Creates inadequate tissue perfusion Cannot be seen Not a specific disease or injury Inadequate flow of blood to the body’s cells and failure to rid the body of metabolic wastes

35 Pathophysiology of Shock (3 of 4)
Diagnosing shock Evaluation of a patient’s level of organ perfusion is important. If conditions causing shock are not promptly addressed, the patient will soon die. Severity of disease or injury overwhelms the normal compensatory mechanisms.

36 Pathophysiology of Shock (4 of 4)
Perfusion depends on: Cardiac output Systematic vascular resistance Transport of oxygen

37 Mechanisms of Shock (1 of 6)
Normal tissue perfusion Requires three intact mechanisms: Heart Blood and body fluids Blood vessels If any one of those mechanisms is damaged, tissue perfusion may be disrupted, and shock will ensue.

38 Mechanisms of Shock (2 of 6)
Cardiogenic shock Arises because of failure of the heart Cardiac arrest is the most drastic form. May occur secondary to: Myocardial infarction Cardiac arrhythmias Pulmonary embolism Severe acidosis A variety of other conditions

39 Mechanisms of Shock (3 of 6)
Hypovolemic shock Occurs because of a loss of fluid volume Lost as blood, plasma, or electrolyte solution Suspect in any patient with unexplained shock. Treat the patient for hypovolemia first.

40 Mechanisms of Shock (4 of 6)
Neurogenic shock Failure of vasoconstriction Sympathetic nervous system ordinarily controls the dilation and constriction. In certain situations Spinal cord injury Pulmonary embolism Gastric overdistention

41 Mechanisms of Shock (5 of 6)
More than one cause More than one component of the circulatory system may be affected in case of shock. Some types of shock always result from combined deficits from both fluid leakage into the interstitial space and vasodilation.

42 Mechanisms of Shock (6 of 6)
High risk Patients known to have had trauma or bleeding Elderly people Patients with massive myocardial infarction Pregnant women Patients with a possible source for septic shock

43 Compensation for Decreased Perfusion (1 of 6)
Maintaining blood pressure Central homeostatic mechanism Baroreceptors Stimulation by systolic pressure between 60 and 80 mm Hg Sympathetic nervous system is also stimulated.

44 Compensation for Decreased Perfusion (2 of 6)
In response to hypoperfusion Renin-angiotensin-aldosterone system Antidiuretic hormone Triggers salt and water retention Increase in blood pressure and cardiac output Spleen releases RBCs that are normally sequestered.

45 Compensation for Decreased Perfusion (3 of 6)
As hypoperfusion persists Myocardial oxygen demand continues to increase. Compensatory mechanisms fail. Myocardial function worsens. Tissue perfusion decreases. Fluid may leak from the blood vessels.

46 Compensation for Decreased Perfusion (4 of 6)
The body’s own “medicines” Epinephrine and norepinephrine Released by the body as part of the global compensatory state Administered by caregivers in cases of anaphylaxis, severe airway disease, and cardiac arrest

47 Compensation for Decreased Perfusion (5 of 6)
The body’s “medicines” (continued) Release of epinephrine improves cardiac output. Alpha-1 response to release of epinephrine includes: Vasoconstriction Increased peripheral vascular resistance Increased afterload from the arteriolar constriction

48 Compensation for Decreased Perfusion (6 of 6)
The body’s “medicines” (continued) Alpha-2 effects ensure a regulated release of alpha-1. Effects of norepinephrine are primarily alpha-1 and alpha-2: Center on vasoconstriction and increasing PVR “Golden hour of trauma”

49 Types of Shock (1 of 4) Impairment of cellular metabolism
Inadequate oxygen and nutrient delivery to the metabolic apparatus Results in the inability to properly use oxygen and glucose

50 Types of Shock (2 of 4) Impairment of cellular metabolism (continued)
Cell converts to anaerobic metabolism Increased lactic acid production and metabolic acidosis Decreased oxygen affinity for hemoglobin Decreased adenosine triphosphate production Changes in cellular electrolytes Cellular edema Release of lysosomal enzymes Elevated blood glucose level

51 Types of Shock (3 of 4) Weil-Shubin classification
Mechanistic point of view Central shock Cardiogenic shock Obstructive shock Peripheral shock Hypovolemic shock Distributive shock

52 Types of Shock (4 of 4) Regardless of type Characterized by:
Reduced cardiac output Circulatory insufficiency Rapid heartbeat Most types also include pallor. Patient’s mental status may be altered. Low blood pressure is a late sign.

53 Cardiogenic Shock (1 of 2)
Heart is unable to maintain adequate peripheral oxygen delivery. Circulation requires the constant pumping. Destruction or inflammation of this muscle If too much muscular damage occurs, the heart no longer functions effectively.

54 Cardiogenic Shock (2 of 2)
Most common causes Extensive infarction of the left ventricle Diffuse ischemia Decompensated congestive heart failure resulting in primary pump failure May be due to a single massive event or from cumulative damage

55 Obstructive Shock Blood flow in the heart or great vessels becomes blocked. Pericardial temponade Aortic dissection Left atrial tumor Large pulmonary embolus or tension pneumothorax

56 Hypovolemic Shock (1 of 6)
Circulating blood volume does not deliver adequate oxygen and nutrients to the body. Most common cause of exogenous is external bleeding due to: Blunt or penetrating injuries Long bone or pelvic fractures Major vascular injuries Multisystem injury

57 Hypovolemic Shock (2 of 6)
Organs and organ systems with a high incidence of exsanguination: Heart Thoracic vascular system Abdominal vascular system Venous system Liver

58 Hypovolemic Shock (3 of 6)
Endogenous occurs when the fluid loss is contained within the body. Dehydration Burn injury Crush injury Anaphylaxis

59 Hypovolemic Shock (4 of 6)
Abnormal losses of fluids and electrolytes GI losses Fever, hyperventilation, or high environmental temperatures Increased sweating Internal losses Plasma losses

60 Hypovolemic Shock (5 of 6)
Fluid loss Therapy aims to restore deficient chemicals. Symptoms of dehydration Loss of appetite Nausea Vomiting Fainting when standing up

61 Hypovolemic Shock (6 of 6)
Physical examination reveals Poor skin turgor Shrunken, furrowed tongue Sunken eyes Pulse will be weak and rapid.

62 Distributive Shock (1 of 5)
Widespread dilation of the resistance or capacitance vessels Circulating blood volume pools in the expanded vascular beds. Three most common types Septic Neurogenic Anaphylactic

63 Distributive Shock (2 of 5)
Septic shock Presence of sepsis syndrome and a systolic blood pressure of less than 90 mm Hg Uncontrolled and unregulated inflammatory-immune response occurs. Insufficient volume of fluid

64 Distributive Shock (3 of 5)
Neurogenic shock Usually results from spinal cord injury Less commonly from medical causes Muscles in the walls of the blood vessels Relative hypovolemia leading to hypotension Skin is pink, warm, and dry. Absence of sweating below the level of injury

65 Distributive Shock (4 of 5)
Spinal shock Local neurologic condition after a spinal injury produces motor and sensory losses May cause significant injury to the autonomic nervous system Swelling and edema of the cord Severe pain above the level of the injury

66 Distributive Shock (5 of 5)
Anaphylactic shock Violent reaction to a foreign substance Patient experiences widespread vascular dilation, resulting in relative hypovolemia. Immune system chemicals are released, causing severe bronchoconstriction.

67 Shock-Related Events (1 of 5)
At the capillary and microcirculatory levels As perfusion decreases Cellular ischemia occurs. Minimal blood flow Cells switch to anaerobic metabolism. Blood stagnates in the capillaries.

68 Shock-Related Events (2 of 5)
Capillary sphincters Circular muscle walls Constrict and dilate Regulate blood flow through the capillary beds Controlled by the autonomic nervous system Regulation is determined by cellular need.

69 Shock-Related Events (3 of 5)
Anaerobic metabolism Body can tolerate for only a limited time. Inefficient Systemic acidosis and depletion of the body’s energy reserves Accumulation of pyruvic acid Increased carbon dioxide production

70 Shock-Related Events (4 of 5)
Intracellular enzymes Digest and neutralize bacteria Bound in a relatively impermeable membrane Cellular flooding explodes the membrane and releases these enzymes. Autodigest the cell

71 Shock-Related Events (5 of 5)
Accumulating acids and waste products Act as potent vasodilators Decrease venous return and diminish blood flow to the vital organs and tissues Cessation of sympathetic nervous system activity Metabolic wastes are released.

72 Multiple-Organ Dysfunction Syndrome (1 of 10)
Progressive condition Combined failure of several organs Major cause of death following septic, traumatic, and burn injuries Classified as primary or secondary Primary is a direct result of an insult. Secondary occurs when injury or infection triggers a massive systemic response.

73 Multiple-Organ Dysfunction Syndrome (2 of 10)
Maldistribution of systemic and organ blood flow Net outcome of overactivity in the systems Often tissues attempt to compensate by accelerating their metabolism. Results in an oxygen supply-demand imbalance

74 Multiple-Organ Dysfunction Syndrome (3 of 10)
Development time Typically within hours to days 14- to 21-day period Cardiovascular collapse and death typically within days to weeks of the initial insult.

75 Multiple-Organ Dysfunction Syndrome (4 of 10)
Specific organs and organ systems Heart Hypoperfusion may stun a healthy heart. Peripheral pulses are weak or absent. Extremities become cyanotic and cold.

76 Multiple-Organ Dysfunction Syndrome (5 of 10)
Lungs Failure evident by adult respiratory distress syndrome or noncardiogenic pulmonary edema. Impaired gas exchange Alveolar cells become ischemic. Respiratory failure, severe hypoxemia, and respiratory acidosis

77 Multiple-Organ Dysfunction Syndrome (6 of 10)
Central nervous system Decreased cerebral perfusion pressure and cerebral blood flow result in confusion, reduced responses to verbal and painful stimuli, and unresponsiveness.

78 Multiple-Organ Dysfunction Syndrome (7 of 10)
Kidneys Reduction in renal blood flow produces acute tubular necrosis leading to oliguria. Toxic waste products cannot be excreted. Metabolic acidosis worsens.

79 Multiple-Organ Dysfunction Syndrome (8 of 10)
Liver Impaired metabolic function and alterations in clotting factors Failure to metabolize waste products Cell death evidenced by an increase in enzyme levels Ischemic hepatitis, hypoxic hepatitis, or shock liver

80 Multiple-Organ Dysfunction Syndrome (9 of 10)
GI tract Results in ischemic gut syndrome Release of vasodilating endotoxins contributes to the progression of shock

81 Multiple-Organ Dysfunction Syndrome (10 of 10)
Signs and symptoms Hypotension Insufficient tissue perfusion Uncontrollable bleeding Multisystem organ failure

82 Phases of Shock (1 of 5) Three successive phases Compensated
Decompensated Irreversible

83 Phases of Shock (2 of 5) Compensated phase of shock Earliest stage
Body can still compensate for blood loss. Level of responsiveness is best indicator of tissue perfusion. Blood pressure is maintained.

84 Phases of Shock (3 of 5) Compensated phase (continued)
Blood loss in hemorrhagic shock can be estimated at 15% to 30%. Narrowing of the pulse pressure occurs. Positive orthostatic tilt test result Treatment will typically result in recovery.

85 Phases of Shock (4 of 5) Decompensated phase of shock
Blood pressure is falling. Blood volume drops by more than 30%. Compensatory measures begin to fail. Signs and symptoms are more obvious. Cardiac output falls dramatically. Treatment will sometimes result in recovery.

86 Phases of Shock (5 of 5) Irreversible (terminal) phase of shock
Arterial blood pressure is abnormally low. Rapid deterioration Life-threatening reductions in cardiac output, blood pressure, and tissue perfusion Cells begin to die. Vital organ damage cannot be repaired.

87 The Clinical Picture of Hypovolemic Shock (1 of 5)
Typical signs and symptoms Inadequate tissue oxygenation and the attempt to compensate Earliest signs of shock are restlessness and anxiety. Decline in tissue perfusion sets off alarms all over the body.

88 The Clinical Picture of Hypovolemic Shock (2 of 5)
Signs and symptoms (continued) A “gut” feeling that something isn’t right If conscious, the patient may complain of thirst and feel nausea. Skin becomes pale, cool, and clammy. Heart speeds up to circulate the remaining RBCs more rapidly.

89 The Clinical Picture of Hypovolemic Shock (3 of 5)
Abdominal trauma Shock may occur without a rapid pulse. Brain signals the respiratory muscles to speed up their activity. As bleeding continues The blood pressure falls. Falling blood pressure is a late sign in shock.

90 The Clinical Picture of Hypovolemic Shock (4 of 5)
Treatment goal Save the brain and kidneys. Best indication of brain perfusion is the state of consciousness. If the patient is conscious and alert If the patient is confused, disoriented, or unconscious

91 The Clinical Picture of Hypovolemic Shock (5 of 5)
Treatment (continued) Kidney perfusion can be gauged by urine output. Adequately perfused kidneys Poorly perfused kidneys shut down. Test for kidney perfusion in the field with capillary refill.

92 General Assessment of a Patient With Suspected Shock (1 of 5)
Assessment plan Scene size-up for hazards BSI precautions Initial assessment Size-up Also includes a quick assessment of the MOI For a patient with suspected shock

93 General Assessment of a Patient With Suspected Shock (2 of 5)
Initial assessment Form a general impression. Assess mental status. Manage ABCs. In conscious patients assess the pulse at the radius. In unconscious patients assess the carotid pulse in the neck. Radial pulse

94 General Assessment of a Patient With Suspected Shock (3 of 5)
Priority Patients with shock will usually be prioritized as “high.” If the shock originates from a medical problem If the shock originates from trauma

95 General Assessment of a Patient With Suspected Shock (4 of 5)
SAMPLE history and baseline vitals Can be done en route to the ED Time is of the essence in shock cases. Keep the on-scene care to essential items. Delay inserting IV lines until en route. Considered hypovolemic or hemorrhagic

96 General Assessment of a Patient With Suspected Shock (5 of 5)

97 Management of a Patient With Suspected Shock (1 of 4)
Airway and ventilation support Take top priority as with any patient Maintain an open airway. Give high-flow supplemental oxygen. Control any external hemorrhage. Try to estimate the amount of blood lost. Look for signs of internal hemorrhage.

98 Management of a Patient With Suspected Shock (2 of 4)
IV fluid therapy Two large-bore catheters Administer IV volume expanders. Solutions of dextrose in water are not effective. Presence of radial pulses equates to systolic blood pressure of 80 to 90 mm Hg.

99 Management of a Patient With Suspected Shock (3 of 4)
PASG/MAST Hypoperfusion with an unstable pelvis Use is controversial. Follow local protocols. Tension pneumothorax Perform needle chest decompression. Cardiac tamponade

100 Management of a Patient With Suspected Shock (4 of 4)
Nonpharmacologic interventions for shock Proper positioning of the patient Prevention of hypothermia Rapid transport Apply the cardiac monitor. Regional trauma center Provide psychological support en route.

101 IV Therapy (1 of 8) Inserted for one of two purposes
Route for immediate replacement of fluid Route for potential fluid replacement IV fluid of choice will be normal saline or lactated Ringer’s.

102 IV Therapy (2 of 8) Hypovolemic shock
All patients need IV fluid replacement. IV access in patients likely to develop hypovolemic shock Profuse external bleeding, internal bleeding, ulcer, vaginal bleeding, Blunt trauma to the abdomen

103 IV Therapy (3 of 8) Patients likely to develop hypovolemic shock (continued) Fracture of the pelvis or femur Severe or widespread burns Heat exhaustion Intractable vomiting or diarrhea Neurogenic or septic shock

104 IV Therapy (4 of 8) Emergency administration of drugs
IV lines should be inserted to keep a vein open. Medication administered directly into the vein ensures that the desired dose of the drug reaches the circulation.

105 IV Therapy (5 of 8) Flow rate Typically determined by local protocol
Usually reflects the presumptive diagnosis and the condition of lungs Takes into account why the IV line was inserted

106 IV Therapy (6 of 8)

107 IV Therapy (7 of 8) Volume expanders and plasma substitutes
Volume expanders are indicated for obstructive and spinal shock. Macromolecular solutions Plasma substitutes Dextran Plasma protein fractions Polygeline

108 IV Therapy (8 of 8) Crystalloids
Solutions that do not contain proteins or other large molecules Fluids of choice when only salt and water have been lost Most commonly used crystalloids Normal saline Lactated Ringer’s solution

109 Management of Specific Types of Shock (1 of 5)
Hypovolemic and hemorrhagic shock Priorities in treating a patient in both types are the same as in treating any other patient. Insert at least one, and preferably two, large-bore peripheral IV lines. If the patient is in critical condition, start the IV en route to the ED.

110 Management of Specific Types of Shock (2 of 5)
Hypovolemic and hemorrhagic shock (continued) Keep the patient at normal temperature. Position Head elevated 15% to 30% Legs propped up 30% on pillows Monitor ECG rhythm, state of consciousness, pulse, and blood pressure.

111 Management of Specific Types of Shock (3 of 5)
Cardiogenic shock Prolonged efforts are not recommended. Time-sensitive patient Supine position Apply ECG electrodes and document the initial rhythm. Auscultate the lungs.

112 Management of Specific Types of Shock (4 of 5)
Neurogenic shock Patient should be immobilized. Keep the patient warm. Use normal saline IV fluid boluses. Use warm fluid to prevent hypothermia.

113 Management of Specific Types of Shock (5 of 5)
Anaphylactic shock Need to act fast Remove the inciting cause if possible. Provide cardiovascular support. Administer epinephrine or a vasopressor. Consider the need for a bronchodilator. Antihistamine

114 Transportation of Patients With Suspected Shock
Transport is inevitable. Questions to be asked are simply when and where. Priority of the patient Availability of a regional trauma center

115 Prevention Strategies
Best prevention Not having the incident Wearing seatbelts Shock and its deadly effects Be alert and search for early signs. Don’t rationalize irregularities away.

116 Summary Anatomy and physiology Pathophysiology of hemorrhage
Assessment and management Shock

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