Seminar On Shock By Dr Abdul Qahar Qureshi
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Transcript of Seminar On Shock By Dr Abdul Qahar Qureshi
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Good morning
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Dept of Oral & Maxillofacial Surgery
Presented by:Dr.Abdul Qahar Qureshi
SHOCK
Presentation of Seminar on
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Contents
Shock- What is it?DefinitionsSignificance of Fluids
& ElectrolytesBlood ComponentsFick PrincipleThe Cardiovascular
System’s & it’s RoleThe Nervous
System & it’s Role
Stages of shockTypes of shockManagement of
ShockRecent Advances in
Management
PART -1 PART -2
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Shock & other termsShock: “The body’s response to poor perfusion”
synonyms: HypoperfusionAcute circulatory collapse
Perfusion: “The process by which oxygenated blood is delivered to the body’s tissue and wastes are removed from the tissue”
Decreased perfusion leads to:Anaerobic metabolismBuild up of toxins
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Significance of Fluids and Electrolytes
Fluids:Water
60%Mixed with proteins and electrolytesSent to various compartments in the body
Intracellular fluid - 75%Extracellular fluid - 25%
Interstitial fluid - 17.5%Intravascular fluid - 7.5%
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ElectrolytesSubstances that dissociate into electrically charged
particles when placed into water.“cations”
Sodium Na+Potassium K+Calcium Ca++Magnesium Mg++
“anions”Chloride Cl-Bicarbonate HCO3-Phosphate PO4-
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“Next of Kin”
N K
ext ra cellular
a+
tra cellular
in +
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CationsSodium (Na+)
Most prevalent cation in the extracellular fluidPlays a major role in regulating the distribution of water
Potassium (K+)Most prevalent cation in the intracellular fluidTransmission of electrical impulses
Calcium (Ca++)Muscle contractionNervous impulse transmission
Magnesium (Mg++)Several biochemical processesClosely associated with phosphate in many processes
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AnionsChloride (Cl-)
Most prevalent anion in the extracellular fluidFluid balance and renal function
Bicarbonate (HCO3-)Principle buffer of the bodyNeutralizes highly acidic hydrogen ion (H+)
Phosphate (HPO4-)Major intracellular anionImportant in body energy storesHelps maintain acid-base balance
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Cellular MembranesPermeability
The degree to which a substance is allowed to pass through a cell membrane
SemipermeableCell membranes that allow only certain
substances to pass through them
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Diffusion
Movement of solutes from an area of greater solute concentration to an area of lower solute concentration
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Osmosis
Movement of water from an area of lower solute concentration to an area of higher solute concentration
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Active TransportMovement of a substance across the
cell membrane against the osmotic gradient
Faster than diffusionRequires energy
Example: Sodium-Potassium Pump
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Facilitated DiffusionRequires the assistance of “helper
proteins”Protein binds to molecule changing it’s
configurationMay or may not require energy
Example: Insulin & Glucose
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Isotonic Solutions
State in which solutions on opposite sides of a semi-permeable membrane are equal in concentration
There is NO fluid shift!
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Hypotonic Solutions
State in which a solution has a lower solute concentration on one side than the other
There is a shift into the intracellular fluid!
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Hypertonic Solutions
State in which a solution has a higher solute concentration on one side than the other
There is a fluid shift into the interstitial fluid!
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Blood Components
Plasma 54%Red Blood Cells
45%White Blood Cells
1%Platelets 1%
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PlasmaFluid portion of bloodContains proteins, carbohydrates, amino acids,
lipids, & mineral saltsErythrocytes
Most numerous cells in bloodCarry hemoglobin
LeukocytesFight infectionProduce antibodies
PlateletsEssential for clot formation
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The Fick Principle
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Fick Principle1. Adequate concentration of inspired
oxygen2. On-loading of oxygen to red blood cells
at lungs3. Delivery of red blood cells to tissue
cells4. Off-loading of oxygen from red blood
cells to tissue cells
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Fick Principle1. Adequate concentration of inspired
oxygen requires:Adequate ventilationHigh concentration of inspired oxygenUnobstructed air passages
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Fick Principle2. On-loading of oxygen to red blood
cells at lungs requires:Minimal obstruction across alveolar-
capillary membrane and Appropriate binding of oxygen to
hemoglobin
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Fick Principle3. Delivery of red blood cells to tissue
cells requires:Normal hemoglobin levelsCirculation of oxygenated cells to
tissues Adequate cardiac functionAdequate volume of blood flowProper routing of blood through
vasculature
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Fick Principle4. Off-loading of oxygen from red blood
cells to tissue cells requires:Close proximity of tissue cells to
capillaries Ideal pH Ideal temperature
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Remove any component from the “Fick Principle” and shock will follow!
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Think in terms of Nutrition!!Cells require a continuous supply of
nutrientsEx: Glucose, Oxygen
Workload demands determine the rate of need
The body automatically adjustsBreakdown of food into energy
AerobicAnaerobic
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Aerobic MetabolismRequired fuels
GlucoseOxygen
Waste productsPyruvic acidCarbon dioxide
Method of excretionRespirationUrination
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Anaerobic MetabolismUses glucose onlyAlmost 20 times less efficient than aerobicCauses dramatic increase in lactic acid production, and
therefore metabolic acidosisVascular dilation follows, causing a further shift in fluids
out of the vascular space and into the interstitial spaceFurther, potassium shifts out of the cell, and sodium in,
which causes cell membrane instability
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Death ComethBrain and Lungs
Die within 4 to 6 minutes without oxygen
OrgansDie within 45 to 90 minutes without oxygen
Skin and muscleDie within 4 to 6 hours without oxygen
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The Pump, The Fluid, & The Container!
The Cardiovascular System’s Role
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The Pump, The Fluid, & The Container!
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The Pump
Blood Pressure
Cardiac OutputSystemic Vascular Resistance
Stroke VolumeHeart Rate
PreloadMyocardial ContractilityAfterload
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Stroke Volume
Amount of blood ejected from the heart with every contraction
Affected by:PreloadContractilityAfterload
Stroke Volume
PreloadMyocardial ContractilityAfterload
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Normal60-100cc per beat for average adult55 cc per beat for child
Ejection FractionPercentage of blood in the ventricle that is ejected during systole, > 50%, or a way to measure the “efficiency” of the “fuel pump”
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Preload Heart muscle is stretched as chambers fill with blood between contractions.
Stretching muscle fibers before contraction increases strength of contraction.
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Influenced by volume of blood returning to heart.More blood returning increases
preload; less blood returning decreases preload.
More stretch of muscles means more forceful contraction.Frank Starling’s Law
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Frank Starling’s LawMore the heart is filled during diastole, the greater the quantity of blood that will be pumped during systole
Increase in volume stretches the heart muscle and increases stroke volume and thus increases cardiac output
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ContractilityContractility is extent and velocity of muscle fiber shortening.
Influenced by:Oxygen supply and demandSympathetic stimulationElectrolyte balanceCalcium
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AfterloadPressure ventricular muscles must generate to overcome higher pressure in aorta.
Greater afterload means harder work for ventricles to eject blood into arteries.
Dictated to large degree by blood pressure.
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Cardiac Output
Amount of blood ejected from the heart each minute
Affected by:Stroke VolumeHeart Rate
Cardiac Output
Stroke VolumeHeart Rate
Cardiac Output = Stroke Volume X Heart Rate
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Blood Pressure
Force that blood exerts against arterial walls
Affected by:Cardiac OutputSystemic Vascular
Resistance
BP
Cardiac OutputSystemic Vascular Resistance
BP = Cardiac Output X Systemic Vascular Resistance
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The FluidSignificant fluid loss
Adult = 1 ½ literChild = ½ literInfant = 100 to 200 mL
Decreased HematocritHemoglobin
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The ContainerContinuous, closed, pressurized pipeline
that moves blood through body.Elastic blood vessels adjust fluid volume
of container.Systemic ControlLocal Control
Affects amount of blood returning to heart and amount of tissue oxygenation.
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The Nervous System & It’s Role!
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ReceptorsSensory nerve endings that sense
changes in blood pressure or carbon dioxide
Baroreceptors (pressure) located in:Aortic archWalls of the atriaVena cavaCarotid sinus
Chemoreceptors (CO2) located in:Brain and spinal cord
Notify the sympathetic nervous system
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Sympathetic Nervous System“Fight or Flight” response
Increases heart rateStimulates the heart to beat more forcefully
Respirations IncreaseRelease of norepinephrine
“Clamps down” on blood vessels Kidneys decrease urinary output to conserve water
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PART -2
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ContentsStages of shockTypes of shockManagement of ShockRecent Advances in Management
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The Stages of ShockCompensated Shock
Also known as nonprogressive Shock
Uncompensated Shock Also known as progressive Shock
Irreversible Shock
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Compensated ShockEarliest phaseUp to 15-25% blood loss Body compensates
Activates the sympathetic nervous system
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Compensated ShockSigns / Symptoms
Altered Level of conciousIncreased pulse rateIncreased respiratory ratePale, cool skin
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Decompensated ShockBlood volume drop greater than 15-25%
Mechanisms no longer able to maintainEven more norepinephrine is released
Cardiac output drops
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Decompensated ShockSigns / Symptoms :
Additional increase in pulse and breathing
Cool, clammy skinDecreased capillary refillNarrowing of pulse pressureSweatingIncreased anxiety and confusionNausea and vomiting
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Irreversible ShockRapid deterioration of the cardiovascular system
Greater blood shunting to heart and brain
Cell death begins
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Irreversible ShockSigns / Symptoms
Marked decrease in level of responsiveness
Decreased respiratory rateProfound hypotensionDecrease in pulse ratePatient has feelings bad
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Types of Shock • Hypovolemic• Septic• Cardiogenic • Anaphylactic• Neurogenic • Obstructive
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Hypovolemic Shock
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Hypovolemic Shock• Non-hemorrhagic
• Vomiting• Diarrhea• Bowel obstruction, pancreatitis• Burns • Dehydration
• Hemorrhagic • GI bleed• Trauma• Massive hemoptysis• Aneurysmal abdominal aortic rupture• Post-partum bleeding
0
20
40
60
80
100
120
Normal 10% 25% 50%
BLOOD LOSS
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Evaluation of Hypovolemic Shock
• CBC• ABG/lactate• Electrolytes• BUN, Creatinine• Coagulation studies
• As indicated• Chest X-ray• Pelvic X-ray• Abd/pelvis CT• Chest CT• GI endoscopy• Bronchoscopy• Vascular radiology
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Septic Shock
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Sepsis• Two or more of SIRS criteria
• Temp > 38 or < 36 C• HR > 90• RR > 20• WBC > 12,000 or < 4,000
• Plus the presumed existence of infection• Blood pressure can be normal!
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Septic Shock• Plus refractory hypotension
• After bolus of 20-40 mL/Kg patient still has one of the following:• SBP < 90 mm Hg • MAP < 65 mm Hg • Decrease of 40 mm Hg from baseline
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Sepsis
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Pathogenesis of Sepsis
Nguyen H et al. Severe Sepsis and Septic-Shock: Review of the Literature and Emergency Department Management Guidelines. Ann Emerg Med. 2006;42:28-54.
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Septic Shock• Clinical signs:
• Hyperthermia or hypothermia• Tachycardia• Wide pulse pressure• Low blood pressure (SBP<90)• Mental status changes• Blood pressure may be “normal”
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Ancillary Studies• Cardiac monitor• Pulse oximetry• CBC, Chem 7, LFTs, Lipase• ABG with lactate• Blood culture , urine culture• CXR• Foley Cathetor
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Examples of septic shock
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Cardiogenic Shock
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Cardiogenic Shock
• Signs:• Cool, mottled skin• Tachypnea • Hypotension• Altered mental status• Narrowed pulse
pressure• Rales, murmur
• Defined as:• SBP < 90 mmHg• CI < 2.2 L/m/m2
• PCWP > 18 mmHg
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Etiologies
• Causes of cardiogenic shock:• AMI• Sepsis• Myocarditis• Myocardial contusion• Aortic or mitral stenosis, • Acute aortic insufficiency
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Pathophysiology of Cardiogenic Shock
• Often after ischemia, loss of LV function• Lose 40% of LV clinical shock ensues
• CO reduction = lactic acidosis, hypoxia• Stroke volume is reduced
• Tachycardia develops as compensation • Ischemia and infarction worsens
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Ancillary Tests• CXR• CBC, Cardiac enzymes, Coagulation
studies• Echocardiogram
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Anaphylactic Shock
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Anaphylactic Shock
• Anaphylaxis – a severe systemic hypersensitivity reaction characterized by multisystem involvement • IgE mediated
• Anaphylactoid reaction – clinically indistinguishable from anaphylaxis, do not require a sensitizing exposure• Not IgE mediated
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Anaphylactic Shock
• Symptoms of anaphylaxis:• First- Pruritus, flushing, urticaria appear
• Next- Throat fullness, anxiety, chest tightness, shortness of breath and lightheadedness
• Finally- Altered mental status, respiratory distress and circulatory collapse
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Anaphylactic Shock• Risk factors for fatal anaphylaxis
• Poorly controlled asthma • Previous anaphylaxis
• Reoccurrence rates• 40-60% for insect stings• 20-40% for radiocontrast agents• 10-20% for penicillin
• Most common causes• Antibiotics• Insects• Food
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Anaphylactic Shock
• Mild, localized urticaria can progress to full anaphylaxis
• Symptoms usually begin within 60 minutes of exposure
• Faster the onset of symptoms = more severe reaction
• Biphasic phenomenon occurs in up to 20% of patients• Symptoms return 3-4 hours after initial reaction has
cleared• A “lump in my throat” and “hoarseness” heralds
life-threatening laryngeal edema
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Anaphylactic Shock- Diagnosis
• Clinical diagnosis• Defined by airway compromise,
hypotension, or involvement of cutaneous, respiratory, or GI systems
• Look for exposure to drug, food, or insect
• Labs have no role
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Anaphylactic shock mechanism
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Neurogenic Shock
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Neurogenic Shock • Occurs after acute spinal cord injury• Sympathetic outflow is disrupted leaving
unopposed vagal tone• Results in hypotension and bradycardia• Spinal shock- temporary loss of spinal
reflex activity below a total or near total spinal cord injury (not the same as neurogenic shock, the terms are not interchangeable)
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Neurogenic Shock • Loss of sympathetic tone results in warm
and dry skin• Shock usually lasts from 1 to 3 weeks• Any injury above T1 can disrupt the entire
sympathetic system• Higher injuries = worse paralysis
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Obstructive Shock
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Obstructive Shock• Tension pneumothorax
• Air trapped in pleural space with 1 way valve, air/pressure builds up
• Mediastinum shifted impeding venous return• Chest pain, SOB, decreased breath sounds• No tests needed!• Rx: Needle decompression, chest tube
Needle decompression
chest tube
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Obstructive Shock• Cardiac tamponade
• Blood in pericardial sac prevents venous return to and contraction of heart
• Related to trauma, pericarditis, MI• Beck’s triad: hypotension, muffled heart
sounds• Diagnosis: large heart CXR• Rx: Pericardiocentisis
Pericardiocentisis
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Management of the Patient in Shock
Work to maintain adequate blood pressure and perfuse vital organs.
Rapid assessment and immediate transportation are essential for patient survival.
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Management of the Patient in ShockEvaluation directed at assessing oxygenation and perfusion of body organs
Goals of pre-hospital care include:Ensuring a patent airwayProviding adequate oxygenation and ventilation
Restoring perfusion
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Level of ConsciousnessAssessed throughout initial survey.
Better indicator of tissue perfusion than most other vital signs.
Assume altered mental status is due to decreased cerebral perfusion.
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Level of ConsciousnessRestlessness or agitationDisorientationConfusionInability to respondCombative behaviorUnresponsive
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AirwayOpening the airway
Head-tilt, chin-liftModified jaw thrust
Sounds that may indicate airway obstruction include:Snoring (tongue)Gurgling (liquids such as blood or
vomitus)Stridor (foreign body/swelling)
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AirwayUse airway adjuncts if necessary. Endotracheal intubation is preferred to prevent aspiration of blood.
Clear blood or fluids with suction.Remove large foreign objects with finger sweep.
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Breathing & Oxygenation
LOOK, LISTEN & FEEL, for air exchange.
RATE, QUALITY & DEPTH of respirations.
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Breathing & OxygenationProvide 100% oxygen with non-
rebreather mask at 10 to 15 L/min.Ensure reservoir remains inflated at
end of each inspiration.For assisted ventilations, supply
100% oxygen via bag-valve-mask.
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CirculationLook for and control obvious
external bleeding.Assess RATE, RHYTHM, & QUALITY
of pulse.Palpable pulse location may provide
estimate of systolic pressure.Note color, appearance, and
temperature of skin.
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CirculationA fast, weak, or thready pulse
suggests decreased circulatory volumeColor, appearance, and temperature of
the skinPaleMottledCyanotic
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CirculationControl any obvious external bleedingDirect pressurePressure pointsTourniquetPASG
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CirculationElevate patient's legs.Apply, and if necessary inflate the pneumatic anti-shock garment.
Place 2 large bore IV lines.
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Pneumatic Anti-Shock Garment
Tool to care for hypotension and shock.
Helps control bleeding by applying pressure to blood vessels.
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PASG IndicationsHypovolemic shock from any cause.Hypotension secondary to decreased cardiac output.
Fracture stabilization.Criteria for PASG include systolic blood pressure below 90 mm Hg with obvious signs and symptoms of shock.
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PASG ContraindicationsPulmonary edema (absolute
contraindication).Abdominal compartment inflation
is contraindicated in:PregnancyRespiratory distress of any natureEviscerationCases of impaled objects in abdomen
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PASG ComplicationsUse in presence of chest injuries.
May increase bleeding in intrathoracic cavity leading to tension hemopneumothorax.
Will increase breathing difficulty in patient with flail segment.
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PASG Pneumatic Anti-Shock Garment
BP to 100 mmHg, or velcro crackles
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Fluid ReplacementIV lines are used to counter blood loss by introducing fluid into intravascular space.
Fluids help restore circulating volume until body can manufacture more blood.
Patient in hypovolemic shock needs at least two IV lines.
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Maintain Body TemperatureMaintain body temperature as close to normal as possible.
Pay attention to:Environmental / Weather ConditionsTemperature of oxygen and IV fluidsLocation of patient
Protect patient from elements.
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Maintain Body TemperatureRemove wet clothing.Cover patient to prevent heat loss.
Too much heat produces vasodilation, counteracting body's vasoconstrictive compensatory efforts.
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DRUGSSedatives- Morphine, Barbiturates andLargactilChronotropic Agents-AtropineInotropic Agents-Dopamine and DobutamineVasodilators-Nitroprusside and NitroglycerinVasocontrictorBeta-blockersDiuretics
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References:
Shwartz:Principles of Surgery,
Guyton & Hall: Medical Physiology,
Sembulingam: Medical Physiology,
Davidson’s :Textbook of Medicine,
Harrison’s :Textbook of Medicine,
Manipal:text book of general surgery.
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HAVE A NICE DAY