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Shock Dr. Tanuj Paul Bhatia
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Definition Inadequate delivery of oxygen and nutrients to maintain normal tissue and cellular function.
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DISTRIBUTION OF BODY FLUIDS
FLUID % OF BODY WEIGHT
Total body water 60%
Intracellular 40%
Extracellular 1.Interstitial 2.Intravascular
20%15%5%
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TYPES OF SHOCK1. Hypovolemic shock2. Septic shock3. Cardiogenic shock4. Neurogenic shock5. Anaphylactic shock
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Hypovolaemic shockMost common form seen clinically.Results from depletion of circulating blood
volume.This may result from
Hemorrhage Plasma loss eg. Burns Loss of ECF eg.
Intestinal fistulas,VomitingDiarrhoea
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Pathophysiology Loss of
circulating blood volume
Diminished venous return
to heart
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Autoregulation Decreased arterial BP
Stimulation of baroreceptors
and chemorecepto
rs
Increased sympathetic
activity
1. Increased heart rate.
2. Inc. Myocardial contractility.
3. Constriction of arterioles.
Cardial output
increases
Protects renal, coronary and
cerebral circulations.
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Other mechanisms Renin from JGA,Angiotensin ,Aldosterone from adrenal cortex,Anti-diuretic hormone from pituitary
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• Despite these adjustments cells become starved.
Anerobic metabolism and lactic acidosis.
Sustained hypoxia.
“Sick cell syndrome”
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Clinical picture
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Mild hypovolaemia Deficit <20% of blood volume.Cool, damp extremities.Patient is thirsty.Maybe chilly.UOP and BP are normal in supine position
but BP may fall on standing.
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Moderate hypovolemiaDeficit of 20%-40% of blood volume.Cold extremities.Thirst.Chills.Moderate tachycardia.Decreased urine output.BP falls in standing position but may be
normal in supine position.
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Severe hypovolaemiaDeficit >40% of blood volume.All above signs.Decreased urinary output.Rapid, thready pulse.Low BP.Restlessness and agitation due to decreased
cerebral perfusion.
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Parameters α competence of circulationLevel of cerebral activity.Hourly urine output (normal = 30-50ml/hr in
adults).Central venous pressure.Normal range of CVP is 3-5 cm of H2O above
the manubriosternal angle.
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Investigations Baseline investigations.ABG = arterial blood gases (pH,pO2,pCO2)ECG monitoring.Serum electrolytes.
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Management Aim – to increase cardiac output and tissue
perfusion.Plan : 1. Tackle the primary problem eg.
Hemorrhage. 2. Adequate fluid replacement. 3. Improving cardiac function with inotropic
drugs. 4. Correcting acid base disturbance and
electrolyte abnormalities.
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Outline of treatment1. Resuscitation = A + B2. Fluid replacement Crystalloid solution used for initial resuscitation. Glucose should not be used as it may cause
diuresis and further depletion of circulating volume.
2 litres of crystalloid are given as fast as possible in sever shock.
Severity of shock determines the rate of fluid. CVP acts as a guideline.3. Positioning: elevation of both legs.
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Classification of hypovolemic Shock
Class EBL Treatment
I <15% (<750ml) Fluids
II 15-30% (750-1.5L) Fluids
III 30-40% (1.5L-2.0L) Fluids + Blood
IV >40% (>2.0L) Fluids + Blood
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Vasopressor drugsUse of vasopressor drugs not recommended
in routine.They raise blood pressure by increasing
peripheral vascular resistance decreasing tissue perfusion.
Inotropic drugs like Dopamine and Dobutamine may need to be used to improve cardiac action.
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Indicators of successful resuscitation1. Warm skin.2. Well perfused skin.3. Urine output 30-60 ml/hr.4. Alert sensorium.
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Venous access1. Peripheral line 2. Central line
Femoral Internal jugular Subclavian
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Parenteral fluid therapyCrystalloids
IsotonicHypertonicHypotonic
Colloids Albumin preperationsDextranHydroxyethyl starch
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Crystalloids Crystalloids are solutions that contain sodium
as the major osmotically active particle.Relatively inexpensiveReadily availableUseful for : - volume expansion - maintenance infusion - correction of electrolyte disorders
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Isotonic crystalloidsE.g.. Lactated ringer’s solution(RL), 0.9%
NaCl(normal saline)Distribute uniformly throughout the ECF.RL mimics ECF and is considered a
BALANCED SALT SOLUTION.RL preferred for replacing GI losses and
extracellular fluid volume losses.Normal Saline preferred in the presence of
hyperkalemia, hypercalcemia, hyponatremia, hypochloremia, or metabolic alkalosis.
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Other crystalloidsHypertonic saline solutions(e.g. 10%NaCl) :
can be used for resuscitation in combination with colloids.
BUT, there is more danger of complications like hypernatremia, hyperchloremia, hypokalemia with rapid infusion.
Hypotonic saline solutions (e.g. 0.45%NaCL): expand the intravascular compartment by as
little as 10% of the volume infused.Not used for resuscitation for the same reason.
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Colloid solutionsContain high–molecular-weight substances
that remain in the intravascular space.Lessens the total amount of fluid needed for
resuscitation.Substantially more expensive than
crystalloids .Indicated when crystalloids fail to sustain
plasma volume because of low colloid osmotic pressure. E.g. Burns.
E.g. Dextran, Albumin preperations, Hydroxyethyl starch.
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Maintenance fluids 100 mL/kg per day for the first 10 kg.50 mL/kg per day for the second 10 kg. 20 mL/kg per day for each subsequent 10 kg.
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Glasgow coma score
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SEPTIC SHOCK
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Septic shockResults either by gram +ve or gram –ve
bacterial infection.Gram –ve sepsis is more dangerous, common
scources of gram –ve organisms are:Genitourinary tractRespiratory tractIntestines.
• Commonly involved gram –ve organisms are E. coli, Proteus, Klebsiella, P. aeruginosa.
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Why is gram negative sepsis becoming more important?There is indiscriminate use of potent
antibiotics now a days.Leads to development of virulent
RESISTANT ORGANISMS. Hospitals are major reservoir of
such infection.This can easily transmit from one
patient to another.
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Pathophysiology of septic shock‘ENDOTOXINS’
Bacterial lipopolysaccharides.
Part of bacterial cell wall.Released mainly when bacteria die.
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These lead to :-Activation of complement, fibrinolytic, kinin
systems,Activation of platelets and neutrophils.Endovascular injury at microvascular level.Sudden release of vasoactive substances from
injured endo. cells .Macrophage stimulation and release of
mediators ( IL-6,TNF,Arachidonic acid metabolites)
All these further lead to more endovascular damage.
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Endothelial injury
Increased microvascular permeability
Transcapillary fluid loss
Decreased cardiac output leading to SHOCK
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Risk factors for septic shock1. Liver failure,2. Immune deficiency,3. Diabetes,4. Malnutrition,5. Long term steroid administration,6. Cytotoxic drugs,7. Massive bacterial load. E.g. intestinal
perforation.
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MOFS/MODSMulti organ failure/dysfunction syndrome.Mediators from neutrophils act in a non
specific fashion, when activated systemically, can produce injury to normal micro-circulation.
Features : Stress ulceration,Biochemical signs of liver failure,Lethargy,May progress to coma and later death.
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Clinical presentation of septic shockEARLY RECOGNITION IS VERY IMPORTANT1. Chills,2. Elevated temperature above 101 F,3. Hyperventilation,4. Oliguria,5. Altered sensorium,6. White blood cell count is raised.
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Management 1. Shift to ICU,2. CVP monitoring,3. Urinary output monitoring,4. IV fluid infusion : RL@20ml/kg bolus.....
further Mx according to CVP.5. Thorough search of the source of infection.6. Drain the infective process as soon and
when possible.
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Pulmonary therapySepsis endothelial damage to pulmonary
capillaries.Pronounced alveolar injury, interstitial
oedema and hemorrhage.Treatment is by maintaining controlled
airway and an assisted ventilation.Not needed if sepsis is controlled early.
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CARDIOGENIC SHOCK
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Etiology 1. Massive myocardial infarction2. Severe valvular heart disease3. Arrhythmias4. Pulmonary embolism – right side of heart
comes under sudden strain.
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Pathogenesis
Ventricular failure
Increased back pressure In pulmonary capillaries
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Diagnosis Previous history of cardiovascular disease,Distended neck veins,Low BP,Peripheral edema,Enlarged and tender liver,Rales on lung auscultation,ECG signs of ischaemia,Enlarged heart on X Ray.
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Treatment Opioids to relieve pain and provide sedation.Diuretics, decrease afterload ,alleviate
peripheral and pulmonary edema.Inotropic drugs improve cardiac contractility.
E.g. dopamine in low doses.Sometimes, Mechanical support to heart with
an intra aortic balloon.
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NEUROGENIC SHOCK
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Neurogenic shockAssociated with :
Stress,
Spinal injury,
High spinal anesthesia.
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Pathogenesis Loss of arterial and venous tone
Peripheral pooling of blood
Fall in venous return and cardiac output
Hypotension
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Vasovagal or psychogenic shock
Also a part of neurogenic shock.
Fainting attack brought about by intense pain or sudden fear.
Onset is alarming but recovery is RAPID.
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Sudden
decrease in
peripheral
vascular
resistance
Pooling of blood in limb muscles
Decrease
d venous
return
Reflex
vagal
action
Bradycardia
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Treatment of neurogenic shockVolume expansion with crystalloids,Vasoconstrictors are useful.Goal is to increase BP to sustain coronary
perfusion.Trendelenburg’s position can be temporarily
useful.Short term steroids may also be useful.
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Anaphylactic shockKnown to follow penicillin injection or
administration of serum.Antigen
combines with IgE
Mast cells and basophils
Release of histamine Bronchospas
m,Laryngeal
edema,Resp.
distress,Massive
vasodilatation
Hypotension and shock
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Treatment of anaphylactic shockAqueous epinephrine 0.5-1 ml of 1:1000
solution given i.v.Repeat dose may be given in 5-10 minutes.Steroids.O2 administration.Volume expandors and pressor agents.
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