Shock Dr. Tanuj Paul Bhatia

Definition Inadequate delivery of oxygen and nutrients to maintain normal tissue and cellular function.

DISTRIBUTION OF BODY FLUIDS

FLUID % OF BODY WEIGHT

Total body water 60%

Intracellular 40%

Extracellular 1.Interstitial 2.Intravascular

20%15%5%

TYPES OF SHOCK1. Hypovolemic shock2. Septic shock3. Cardiogenic shock4. Neurogenic shock5. Anaphylactic shock

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

Pathophysiology Loss of

circulating blood volume

Diminished venous return

to heart

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.

Other mechanisms Renin from JGA,Angiotensin ,Aldosterone from adrenal cortex,Anti-diuretic hormone from pituitary

• Despite these adjustments cells become starved.

Anerobic metabolism and lactic acidosis.

Sustained hypoxia.

“Sick cell syndrome”

Clinical picture

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.

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.

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.

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.

Investigations Baseline investigations.ABG = arterial blood gases (pH,pO2,pCO2)ECG monitoring.Serum electrolytes.

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.

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.

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

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.

Indicators of successful resuscitation1. Warm skin.2. Well perfused skin.3. Urine output 30-60 ml/hr.4. Alert sensorium.

Venous access1. Peripheral line 2. Central line

Femoral Internal jugular Subclavian

Parenteral fluid therapyCrystalloids

IsotonicHypertonicHypotonic

Colloids Albumin preperationsDextranHydroxyethyl starch

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

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.

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.

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.

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

SEPTIC SHOCK

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.

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.

Pathophysiology of septic shock‘ENDOTOXINS’

Bacterial lipopolysaccharides.

Part of bacterial cell wall.Released mainly when bacteria die.

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.

Endothelial injury

Increased microvascular permeability

Transcapillary fluid loss

Decreased cardiac output leading to SHOCK

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.

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.

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.

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.

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.

CARDIOGENIC SHOCK

Etiology 1. Massive myocardial infarction2. Severe valvular heart disease3. Arrhythmias4. Pulmonary embolism – right side of heart

comes under sudden strain.

Pathogenesis

Ventricular failure

Increased back pressure In pulmonary capillaries

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.

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.

NEUROGENIC SHOCK

Neurogenic shockAssociated with :

Stress,

Spinal injury,

High spinal anesthesia.

Pathogenesis Loss of arterial and venous tone

Peripheral pooling of blood

Fall in venous return and cardiac output

Hypotension

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.

Sudden

decrease in

peripheral

vascular

resistance

Pooling of blood in limb muscles

Decrease

d venous

return

Reflex

vagal

action

Bradycardia

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.

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

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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