1 Pathophysiology of Hemorrhage Simply means bleedingCan range from a “nick,” to a severely spurting artery, to a ruptured spleenExternal bleeding (visible hemorrhage)Internal bleeding
2 External Hemorrhage (1 of 2) External bleedingUsually due to a break in the skinExtent or severityBleeding from a capillaryBleeding from a veinBleeding from an artery
3 External Hemorrhage (2 of 2) InjuriesDo not always have serious hemorrhagingOther injuries may cause more bleeding than expected.
4 Internal Hemorrhage (1 of 3) Internal bleedingAs a result of traumaNontraumaticCases of GI bleeding from the upper or lower GI tractRuptured ectopic pregnanciesRuptured aneurysms
5 Internal Hemorrhage (2 of 3) Must be treated promptlySigns 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) ManagementFocuses on:Treatment of shockMinimizing movement of the injured or bleeding part or regionRapid transportEventually will need a surgical procedure to stop the bleeding
7 Controlled Versus Uncontrolled Hemorrhage (1 of 3) Serious emergencySearch for life-threatening bleeding.If the hemorrhage cannot be controlled in the fieldConcentrate on attempting to control the bleeding as you rapidly transport the patient
8 Controlled Versus Uncontrolled Hemorrhage (2 of 3) External bleedingMost can be managed with direct pressureArterial 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 bleedingMost cases are rarely fully controlled in the prehospital setting.Rapid transportPneumatic antishock garment/military antishock trousers (PASG/MAST)
10 The Significance of Bleeding (1 of 5) Blood lossOften difficult to determineLooks different on different surfacesPatient’s presentation and your assessment direct your care.
11 The Significance of Bleeding (2 of 5) AveragesHuman 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 ratesDecreasing blood pressureInfants and children
13 The Significance of Bleeding (4 of 5) CompensationDepends on the rate of bleedingHealthy 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 presentA significant MOIPoor general appearance of the patientSigns and symptoms of shockSignificant amount of blood lossRapid blood lossUncontrollable bleeding
15 Physiologic Response to Hemorrhage (1 of 4) Bleeding from an arteryBright redSpurts in time with the pulseDifficult to controlBleeding from an open veinMuch darkerFlows steadilyEasier to manage
16 Physiologic Response to Hemorrhage (2 of 4) Bleeding from damaged capillary vesselsDark redOozes steadily but slowlyVenous and capillary bleeding is more likely to clot spontaneously.On its ownBleeding tends to stop rather quickly.Response to internal clotting mechanisms and exposure to air
17 Physiologic Response to Hemorrhage (3 of 4) HemostasisWhen vessels are laceratedOpen 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 failMedicationsSevere injuryOnly 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-upBegins assessment of any patientGeneral impression and initial assessment once the scene is deemed safe to enterBSIGlovesMaskEyeshieldGown
20 Assessment of a Bleeding Patient (2 of 5) Initial assessmentDetermine 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) MOITrauma patientsMay be best indicator of internal injury or bleeding
22 Assessment of a Bleeding Patient (4 of 5) Focused historyElaborate 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 examNote the color of bleeding.Try to determine its source.Coffee-ground emesisMelenaHematocheziaHematuriaNonmenstrual vaginal bleeding
24 Management of a Bleeding Patient (1 of 3) Managing external hemorrhageSteps to control hemorrhagingApply 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 mouthEpistaxisMay indicate a skull fractureApplying 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 areasControl 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) FracturesMost 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 splintsCan control the bleeding associated with severe soft-tissue injuries or fracturesStabilize fracturesAct like a pressure dressing applied to an entire extremity rather than to a small, local areaMonitor circulationNot appropriate for use on arterial bleeding
29 Special Management Techniques (3 of 3) HemostatsMay be helpful when a vessel has been severedSimply apply hemostats to the ends of the vessel.TourniquetsUse 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 managementOccurs in the hospitalPrehospital managementTreating 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 hemorrhageNot whether the patient will be transportedHow fast the decision should be madeWhere the patient should be taken
33 Pathophysiology of Shock (1 of 4) HypoperfusionOccurs when the level of tissue perfusion decreases below normalEarly 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 systemCreates inadequate tissue perfusionCannot be seenNot a specific disease or injuryInadequate 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 shockEvaluation 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 outputSystematic vascular resistanceTransport of oxygen
37 Mechanisms of Shock (1 of 6) Normal tissue perfusionRequires three intact mechanisms:HeartBlood and body fluidsBlood vesselsIf any one of those mechanisms is damaged, tissue perfusion may be disrupted, and shock will ensue.
38 Mechanisms of Shock (2 of 6) Cardiogenic shockArises because of failure of the heartCardiac arrest is the most drastic form.May occur secondary to:Myocardial infarctionCardiac arrhythmiasPulmonary embolismSevere acidosisA variety of other conditions
39 Mechanisms of Shock (3 of 6) Hypovolemic shockOccurs because of a loss of fluid volumeLost as blood, plasma, or electrolyte solutionSuspect in any patient with unexplained shock.Treat the patient for hypovolemia first.
40 Mechanisms of Shock (4 of 6) Neurogenic shockFailure of vasoconstrictionSympathetic nervous system ordinarily controls the dilation and constriction.In certain situationsSpinal cord injuryPulmonary embolismGastric overdistention
41 Mechanisms of Shock (5 of 6) More than one causeMore 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 riskPatients known to have had trauma or bleedingElderly peoplePatients with massive myocardial infarctionPregnant womenPatients with a possible source for septic shock
43 Compensation for Decreased Perfusion (1 of 6) Maintaining blood pressureCentral homeostatic mechanismBaroreceptorsStimulation by systolic pressure between 60 and 80 mm HgSympathetic nervous system is also stimulated.
44 Compensation for Decreased Perfusion (2 of 6) In response to hypoperfusionRenin-angiotensin-aldosterone systemAntidiuretic hormoneTriggers salt and water retentionIncrease in blood pressure and cardiac outputSpleen releases RBCs that are normally sequestered.
45 Compensation for Decreased Perfusion (3 of 6) As hypoperfusion persistsMyocardial 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 norepinephrineReleased by the body as part of the global compensatory stateAdministered 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:VasoconstrictionIncreased peripheral vascular resistanceIncreased 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 apparatusResults 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 metabolismIncreased lactic acid production and metabolic acidosisDecreased oxygen affinity for hemoglobinDecreased adenosine triphosphate productionChanges in cellular electrolytesCellular edemaRelease of lysosomal enzymesElevated blood glucose level
51 Types of Shock (3 of 4) Weil-Shubin classification Mechanistic point of viewCentral shockCardiogenic shockObstructive shockPeripheral shockHypovolemic shockDistributive shock
52 Types of Shock (4 of 4) Regardless of type Characterized by: Reduced cardiac outputCirculatory insufficiencyRapid heartbeatMost 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 muscleIf too much muscular damage occurs, the heart no longer functions effectively.
54 Cardiogenic Shock (2 of 2) Most common causesExtensive infarction of the left ventricleDiffuse ischemiaDecompensated congestive heart failure resulting in primary pump failureMay be due to a single massive event or from cumulative damage
55 Obstructive ShockBlood flow in the heart or great vessels becomes blocked.Pericardial temponadeAortic dissectionLeft atrial tumorLarge 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 injuriesLong bone or pelvic fracturesMajor vascular injuriesMultisystem injury
57 Hypovolemic Shock (2 of 6) Organs and organ systems with a high incidence of exsanguination:HeartThoracic vascular systemAbdominal vascular systemVenous systemLiver
58 Hypovolemic Shock (3 of 6) Endogenous occurs when the fluid loss is contained within the body.DehydrationBurn injuryCrush injuryAnaphylaxis
59 Hypovolemic Shock (4 of 6) Abnormal losses of fluids and electrolytesGI lossesFever, hyperventilation, or high environmental temperaturesIncreased sweatingInternal lossesPlasma losses
60 Hypovolemic Shock (5 of 6) Fluid lossTherapy aims to restore deficient chemicals.Symptoms of dehydrationLoss of appetiteNauseaVomitingFainting when standing up
61 Hypovolemic Shock (6 of 6) Physical examination revealsPoor skin turgorShrunken, furrowed tongueSunken eyesPulse will be weak and rapid.
62 Distributive Shock (1 of 5) Widespread dilation of the resistance or capacitance vesselsCirculating blood volume pools in the expanded vascular beds.Three most common typesSepticNeurogenicAnaphylactic
63 Distributive Shock (2 of 5) Septic shockPresence of sepsis syndrome and a systolic blood pressure of less than 90 mm HgUncontrolled and unregulated inflammatory-immune response occurs.Insufficient volume of fluid
64 Distributive Shock (3 of 5) Neurogenic shockUsually results from spinal cord injuryLess commonly from medical causesMuscles in the walls of the blood vesselsRelative hypovolemia leading to hypotensionSkin is pink, warm, and dry.Absence of sweating below the level of injury
65 Distributive Shock (4 of 5) Spinal shockLocal neurologic condition after a spinal injury produces motor and sensory lossesMay cause significant injury to the autonomic nervous systemSwelling and edema of the cordSevere pain above the level of the injury
66 Distributive Shock (5 of 5) Anaphylactic shockViolent reaction to a foreign substancePatient 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 levelsAs perfusion decreasesCellular ischemia occurs.Minimal blood flowCells switch to anaerobic metabolism.Blood stagnates in the capillaries.
68 Shock-Related Events (2 of 5) Capillary sphinctersCircular muscle wallsConstrict and dilateRegulate blood flow through the capillary bedsControlled by the autonomic nervous systemRegulation is determined by cellular need.
69 Shock-Related Events (3 of 5) Anaerobic metabolismBody can tolerate for only a limited time.InefficientSystemic acidosis and depletion of the body’s energy reservesAccumulation of pyruvic acidIncreased carbon dioxide production
70 Shock-Related Events (4 of 5) Intracellular enzymesDigest and neutralize bacteriaBound in a relatively impermeable membraneCellular flooding explodes the membrane and releases these enzymes.Autodigest the cell
71 Shock-Related Events (5 of 5) Accumulating acids and waste productsAct as potent vasodilatorsDecrease venous return and diminish blood flow to the vital organs and tissuesCessation of sympathetic nervous system activityMetabolic wastes are released.
72 Multiple-Organ Dysfunction Syndrome (1 of 10) Progressive conditionCombined failure of several organsMajor cause of death following septic, traumatic, and burn injuriesClassified as primary or secondaryPrimary 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 flowNet outcome of overactivity in the systemsOften tissues attempt to compensate by accelerating their metabolism.Results in an oxygen supply-demand imbalance
74 Multiple-Organ Dysfunction Syndrome (3 of 10) Development timeTypically within hours to days14- to 21-day periodCardiovascular collapse and death typically within days to weeks of the initial insult.
75 Multiple-Organ Dysfunction Syndrome (4 of 10) Specific organs and organ systemsHeartHypoperfusion may stun a healthy heart.Peripheral pulses are weak or absent.Extremities become cyanotic and cold.
76 Multiple-Organ Dysfunction Syndrome (5 of 10) LungsFailure evident by adult respiratory distress syndrome or noncardiogenic pulmonary edema.Impaired gas exchangeAlveolar cells become ischemic.Respiratory failure, severe hypoxemia, and respiratory acidosis
77 Multiple-Organ Dysfunction Syndrome (6 of 10) Central nervous systemDecreased 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) KidneysReduction 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) LiverImpaired metabolic function and alterations in clotting factorsFailure to metabolize waste productsCell death evidenced by an increase in enzyme levelsIschemic hepatitis, hypoxic hepatitis, or shock liver
80 Multiple-Organ Dysfunction Syndrome (9 of 10) GI tractResults in ischemic gut syndromeRelease of vasodilating endotoxins contributes to the progression of shock
81 Multiple-Organ Dysfunction Syndrome (10 of 10) Signs and symptomsHypotensionInsufficient tissue perfusionUncontrollable bleedingMultisystem organ failure
82 Phases of Shock (1 of 5) Three successive phases Compensated DecompensatedIrreversible
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 resultTreatment 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 deteriorationLife-threatening reductions in cardiac output, blood pressure, and tissue perfusionCells begin to die.Vital organ damage cannot be repaired.
87 The Clinical Picture of Hypovolemic Shock (1 of 5) Typical signs and symptomsInadequate tissue oxygenation and the attempt to compensateEarliest 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 rightIf 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 traumaShock may occur without a rapid pulse.Brain signals the respiratory muscles to speed up their activity.As bleeding continuesThe blood pressure falls.Falling blood pressure is a late sign in shock.
90 The Clinical Picture of Hypovolemic Shock (4 of 5) Treatment goalSave the brain and kidneys.Best indication of brain perfusion is the state of consciousness.If the patient is conscious and alertIf 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 kidneysPoorly 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 planScene size-up for hazardsBSI precautionsInitial assessmentSize-upAlso includes a quick assessment of the MOIFor a patient with suspected shock
93 General Assessment of a Patient With Suspected Shock (2 of 5) Initial assessmentForm 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) PriorityPatients with shock will usually be prioritized as “high.”If the shock originates from a medical problemIf the shock originates from trauma
95 General Assessment of a Patient With Suspected Shock (4 of 5) SAMPLE history and baseline vitalsCan be done en route to the EDTime 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 supportTake top priority as with any patientMaintain 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 therapyTwo large-bore cathetersAdminister 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/MASTHypoperfusion with an unstable pelvisUse is controversial.Follow local protocols.Tension pneumothoraxPerform needle chest decompression.Cardiac tamponade
100 Management of a Patient With Suspected Shock (4 of 4) Nonpharmacologic interventions for shockProper positioning of the patientPrevention of hypothermiaRapid transportApply the cardiac monitor.Regional trauma centerProvide psychological support en route.
101 IV Therapy (1 of 8) Inserted for one of two purposes Route for immediate replacement of fluidRoute for potential fluid replacementIV 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 shockProfuse 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 femurSevere or widespread burnsHeat exhaustionIntractable vomiting or diarrheaNeurogenic 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 lungsTakes into account why the IV line was inserted
107 IV Therapy (7 of 8) Volume expanders and plasma substitutes Volume expanders are indicated for obstructive and spinal shock.Macromolecular solutionsPlasma substitutesDextranPlasma protein fractionsPolygeline
108 IV Therapy (8 of 8) Crystalloids Solutions that do not contain proteins or other large moleculesFluids of choice when only salt and water have been lostMost commonly used crystalloidsNormal salineLactated Ringer’s solution
109 Management of Specific Types of Shock (1 of 5) Hypovolemic and hemorrhagic shockPriorities 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.PositionHead elevated 15% to 30%Legs propped up 30% on pillowsMonitor ECG rhythm, state of consciousness, pulse, and blood pressure.
111 Management of Specific Types of Shock (3 of 5) Cardiogenic shockProlonged efforts are not recommended.Time-sensitive patientSupine positionApply ECG electrodes and document the initial rhythm.Auscultate the lungs.
112 Management of Specific Types of Shock (4 of 5) Neurogenic shockPatient 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 shockNeed to act fastRemove 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 patientAvailability of a regional trauma center
115 Prevention Strategies Best preventionNot having the incidentWearing seatbeltsShock and its deadly effectsBe alert and search for early signs.Don’t rationalize irregularities away.
116 Summary Anatomy and physiology Pathophysiology of hemorrhage Assessment and managementShock