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Seminar On Shock By Dr Abdul Qahar Qureshi

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Page 1: Seminar On Shock By Dr Abdul Qahar Qureshi

Good morning

Page 2: Seminar On Shock By Dr Abdul Qahar Qureshi

Dept of Oral & Maxillofacial Surgery

Presented by:Dr.Abdul Qahar Qureshi

SHOCK

Presentation of Seminar on

Page 3: Seminar On Shock By Dr Abdul Qahar Qureshi

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

Page 4: Seminar On Shock By Dr Abdul Qahar Qureshi

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

Page 5: Seminar On Shock By Dr Abdul Qahar Qureshi

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%

Page 6: Seminar On Shock By Dr Abdul Qahar Qureshi

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-

Page 7: Seminar On Shock By Dr Abdul Qahar Qureshi

“Next of Kin”

N K

ext ra cellular

a+

tra cellular

in +

Page 8: Seminar On Shock By Dr Abdul Qahar Qureshi

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

Page 9: Seminar On Shock By Dr Abdul Qahar Qureshi

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

Page 10: Seminar On Shock By Dr Abdul Qahar Qureshi

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

Page 11: Seminar On Shock By Dr Abdul Qahar Qureshi

Diffusion

Movement of solutes from an area of greater solute concentration to an area of lower solute concentration

Page 12: Seminar On Shock By Dr Abdul Qahar Qureshi

Osmosis

Movement of water from an area of lower solute concentration to an area of higher solute concentration

Page 13: Seminar On Shock By Dr Abdul Qahar Qureshi

Active TransportMovement of a substance across the

cell membrane against the osmotic gradient

Faster than diffusionRequires energy

Example: Sodium-Potassium Pump

Page 14: Seminar On Shock By Dr Abdul Qahar Qureshi

Facilitated DiffusionRequires the assistance of “helper

proteins”Protein binds to molecule changing it’s

configurationMay or may not require energy

Example: Insulin & Glucose

Page 15: Seminar On Shock By Dr Abdul Qahar Qureshi

Isotonic Solutions

State in which solutions on opposite sides of a semi-permeable membrane are equal in concentration

There is NO fluid shift!

Page 16: Seminar On Shock By Dr Abdul Qahar Qureshi

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!

Page 17: Seminar On Shock By Dr Abdul Qahar Qureshi

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!

Page 18: Seminar On Shock By Dr Abdul Qahar Qureshi

Blood Components

Plasma 54%Red Blood Cells

45%White Blood Cells

1%Platelets 1%

Page 19: Seminar On Shock By Dr Abdul Qahar Qureshi

PlasmaFluid portion of bloodContains proteins, carbohydrates, amino acids,

lipids, & mineral saltsErythrocytes

Most numerous cells in bloodCarry hemoglobin

LeukocytesFight infectionProduce antibodies

PlateletsEssential for clot formation

Page 20: Seminar On Shock By Dr Abdul Qahar Qureshi

The Fick Principle

Page 21: Seminar On Shock By Dr Abdul Qahar Qureshi

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

Page 22: Seminar On Shock By Dr Abdul Qahar Qureshi

Fick Principle1. Adequate concentration of inspired

oxygen requires:Adequate ventilationHigh concentration of inspired oxygenUnobstructed air passages

Page 23: Seminar On Shock By Dr Abdul Qahar Qureshi

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

Page 24: Seminar On Shock By Dr Abdul Qahar Qureshi

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

Page 25: Seminar On Shock By Dr Abdul Qahar Qureshi

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

Page 26: Seminar On Shock By Dr Abdul Qahar Qureshi

Remove any component from the “Fick Principle” and shock will follow!

Page 27: Seminar On Shock By Dr Abdul Qahar Qureshi

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

Page 28: Seminar On Shock By Dr Abdul Qahar Qureshi

Aerobic MetabolismRequired fuels

GlucoseOxygen

Waste productsPyruvic acidCarbon dioxide

Method of excretionRespirationUrination

Page 29: Seminar On Shock By Dr Abdul Qahar Qureshi

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

Page 30: Seminar On Shock By Dr Abdul Qahar Qureshi

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

Page 31: Seminar On Shock By Dr Abdul Qahar Qureshi

The Pump, The Fluid, & The Container!

The Cardiovascular System’s Role

Page 32: Seminar On Shock By Dr Abdul Qahar Qureshi

The Pump, The Fluid, & The Container!

Page 33: Seminar On Shock By Dr Abdul Qahar Qureshi

The Pump

Blood Pressure

Cardiac OutputSystemic Vascular Resistance

Stroke VolumeHeart Rate

PreloadMyocardial ContractilityAfterload

Page 34: Seminar On Shock By Dr Abdul Qahar Qureshi

Stroke Volume

Amount of blood ejected from the heart with every contraction

Affected by:PreloadContractilityAfterload

Stroke Volume

PreloadMyocardial ContractilityAfterload

Page 35: Seminar On Shock By Dr Abdul Qahar Qureshi

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”

Page 36: Seminar On Shock By Dr Abdul Qahar Qureshi

Preload Heart muscle is stretched as chambers fill with blood between contractions.

Stretching muscle fibers before contraction increases strength of contraction.

Page 37: Seminar On Shock By Dr Abdul Qahar Qureshi

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

Page 38: Seminar On Shock By Dr Abdul Qahar Qureshi

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

Page 39: Seminar On Shock By Dr Abdul Qahar Qureshi

ContractilityContractility is extent and velocity of muscle fiber shortening.

Influenced by:Oxygen supply and demandSympathetic stimulationElectrolyte balanceCalcium

Page 40: Seminar On Shock By Dr Abdul Qahar Qureshi

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.

Page 41: Seminar On Shock By Dr Abdul Qahar Qureshi

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

Page 42: Seminar On Shock By Dr Abdul Qahar Qureshi

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

Page 43: Seminar On Shock By Dr Abdul Qahar Qureshi

The FluidSignificant fluid loss

Adult = 1 ½ literChild = ½ literInfant = 100 to 200 mL

Decreased HematocritHemoglobin

Page 44: Seminar On Shock By Dr Abdul Qahar Qureshi

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.

Page 45: Seminar On Shock By Dr Abdul Qahar Qureshi

The Nervous System & It’s Role!

Page 46: Seminar On Shock By Dr Abdul Qahar Qureshi

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

Page 47: Seminar On Shock By Dr Abdul Qahar Qureshi

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

Page 48: Seminar On Shock By Dr Abdul Qahar Qureshi

PART -2

Page 49: Seminar On Shock By Dr Abdul Qahar Qureshi

ContentsStages of shockTypes of shockManagement of ShockRecent Advances in Management

Page 50: Seminar On Shock By Dr Abdul Qahar Qureshi

The Stages of ShockCompensated Shock

Also known as nonprogressive Shock

Uncompensated Shock Also known as progressive Shock

Irreversible Shock

Page 51: Seminar On Shock By Dr Abdul Qahar Qureshi

Compensated ShockEarliest phaseUp to 15-25% blood loss Body compensates

Activates the sympathetic nervous system

Page 52: Seminar On Shock By Dr Abdul Qahar Qureshi

Compensated ShockSigns / Symptoms

Altered Level of conciousIncreased pulse rateIncreased respiratory ratePale, cool skin

Page 53: Seminar On Shock By Dr Abdul Qahar Qureshi

Decompensated ShockBlood volume drop greater than 15-25%

Mechanisms no longer able to maintainEven more norepinephrine is released

Cardiac output drops

Page 54: Seminar On Shock By Dr Abdul Qahar Qureshi

Decompensated ShockSigns / Symptoms :

Additional increase in pulse and breathing

Cool, clammy skinDecreased capillary refillNarrowing of pulse pressureSweatingIncreased anxiety and confusionNausea and vomiting

Page 55: Seminar On Shock By Dr Abdul Qahar Qureshi

Irreversible ShockRapid deterioration of the cardiovascular system

Greater blood shunting to heart and brain

Cell death begins

Page 56: Seminar On Shock By Dr Abdul Qahar Qureshi

Irreversible ShockSigns / Symptoms

Marked decrease in level of responsiveness

Decreased respiratory rateProfound hypotensionDecrease in pulse ratePatient has feelings bad

Page 57: Seminar On Shock By Dr Abdul Qahar Qureshi

Types of Shock • Hypovolemic• Septic• Cardiogenic • Anaphylactic• Neurogenic • Obstructive

Page 58: Seminar On Shock By Dr Abdul Qahar Qureshi

Hypovolemic Shock

Page 59: Seminar On Shock By Dr Abdul Qahar Qureshi

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

Page 60: Seminar On Shock By Dr Abdul Qahar Qureshi

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

Page 61: Seminar On Shock By Dr Abdul Qahar Qureshi

Septic Shock

Page 62: Seminar On Shock By Dr Abdul Qahar Qureshi

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!

Page 63: Seminar On Shock By Dr Abdul Qahar Qureshi

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

Page 64: Seminar On Shock By Dr Abdul Qahar Qureshi

Sepsis

Page 65: Seminar On Shock By Dr Abdul Qahar Qureshi

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.

Page 66: Seminar On Shock By Dr Abdul Qahar Qureshi

Septic Shock• Clinical signs:

• Hyperthermia or hypothermia• Tachycardia• Wide pulse pressure• Low blood pressure (SBP<90)• Mental status changes• Blood pressure may be “normal”

Page 67: Seminar On Shock By Dr Abdul Qahar Qureshi

Ancillary Studies• Cardiac monitor• Pulse oximetry• CBC, Chem 7, LFTs, Lipase• ABG with lactate• Blood culture , urine culture• CXR• Foley Cathetor

Page 68: Seminar On Shock By Dr Abdul Qahar Qureshi

Examples of septic shock

Page 69: Seminar On Shock By Dr Abdul Qahar Qureshi

Cardiogenic Shock

Page 70: Seminar On Shock By Dr Abdul Qahar Qureshi

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

Page 71: Seminar On Shock By Dr Abdul Qahar Qureshi

Etiologies

• Causes of cardiogenic shock:• AMI• Sepsis• Myocarditis• Myocardial contusion• Aortic or mitral stenosis, • Acute aortic insufficiency

Page 72: Seminar On Shock By Dr Abdul Qahar Qureshi

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

Page 73: Seminar On Shock By Dr Abdul Qahar Qureshi

Ancillary Tests• CXR• CBC, Cardiac enzymes, Coagulation

studies• Echocardiogram

Page 74: Seminar On Shock By Dr Abdul Qahar Qureshi

Anaphylactic Shock

Page 75: Seminar On Shock By Dr Abdul Qahar Qureshi

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

Page 76: Seminar On Shock By Dr Abdul Qahar Qureshi

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

Page 77: Seminar On Shock By Dr Abdul Qahar Qureshi

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

Page 78: Seminar On Shock By Dr Abdul Qahar Qureshi

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

Page 79: Seminar On Shock By Dr Abdul Qahar Qureshi

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

Page 80: Seminar On Shock By Dr Abdul Qahar Qureshi

Anaphylactic shock mechanism

Page 81: Seminar On Shock By Dr Abdul Qahar Qureshi

Neurogenic Shock

Page 82: Seminar On Shock By Dr Abdul Qahar Qureshi

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)

Page 83: Seminar On Shock By Dr Abdul Qahar Qureshi

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

Page 84: Seminar On Shock By Dr Abdul Qahar Qureshi

Obstructive Shock

Page 85: Seminar On Shock By Dr Abdul Qahar Qureshi

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

Page 86: Seminar On Shock By Dr Abdul Qahar Qureshi

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

Page 87: Seminar On Shock By Dr Abdul Qahar Qureshi

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.

Page 88: Seminar On Shock By Dr Abdul Qahar Qureshi

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

Page 89: Seminar On Shock By Dr Abdul Qahar Qureshi

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.

Page 90: Seminar On Shock By Dr Abdul Qahar Qureshi

Level of ConsciousnessRestlessness or agitationDisorientationConfusionInability to respondCombative behaviorUnresponsive

Page 91: Seminar On Shock By Dr Abdul Qahar Qureshi

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.

Page 93: Seminar On Shock By Dr Abdul Qahar Qureshi

Breathing & Oxygenation

LOOK, LISTEN & FEEL, for air exchange.

RATE, QUALITY & DEPTH of respirations.

Page 94: Seminar On Shock By Dr Abdul Qahar Qureshi

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.

Page 95: Seminar On Shock By Dr Abdul Qahar Qureshi

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.

Page 96: Seminar On Shock By Dr Abdul Qahar Qureshi

CirculationA fast, weak, or thready pulse

suggests decreased circulatory volumeColor, appearance, and temperature of

the skinPaleMottledCyanotic

Page 97: Seminar On Shock By Dr Abdul Qahar Qureshi

CirculationControl any obvious external bleedingDirect pressurePressure pointsTourniquetPASG

Page 98: Seminar On Shock By Dr Abdul Qahar Qureshi

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.

Page 100: Seminar On Shock By Dr Abdul Qahar Qureshi

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.

Page 101: Seminar On Shock By Dr Abdul Qahar Qureshi

PASG ContraindicationsPulmonary edema (absolute

contraindication).Abdominal compartment inflation

is contraindicated in:PregnancyRespiratory distress of any natureEviscerationCases of impaled objects in abdomen

Page 102: Seminar On Shock By Dr Abdul Qahar Qureshi

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.

Page 103: Seminar On Shock By Dr Abdul Qahar Qureshi

PASG Pneumatic Anti-Shock Garment

BP to 100 mmHg, or velcro crackles

Page 104: Seminar On Shock By Dr Abdul Qahar Qureshi

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.

Page 105: Seminar On Shock By Dr Abdul Qahar Qureshi

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.

Page 107: Seminar On Shock By Dr Abdul Qahar Qureshi

DRUGSSedatives- Morphine, Barbiturates andLargactilChronotropic Agents-AtropineInotropic Agents-Dopamine and DobutamineVasodilators-Nitroprusside and NitroglycerinVasocontrictorBeta-blockersDiuretics

Page 108: Seminar On Shock By Dr Abdul Qahar Qureshi

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.

Page 109: Seminar On Shock By Dr Abdul Qahar Qureshi

HAVE A NICE DAY