SHOCK

DEFINATION- Shock is a state of poor tissue = perfusion with=20 impared cellular metabolism leading to serious pathophysiological = abnormality.=20 This life threatning situation is called Shock.

=20 Maintainence of proper blood circulation depends on three = factors=97

A. =20 Cardiac Function.

B. =20 Capacity of Vascular bed

C. =20 Circulating blood Volume

Defect of any of these leads to shock.

There is a generalized misunderstanding that shock = means=20 haemorrhage and haemorrhage means shock. But there are other causes of=20 shock.

TYPE OF=20 SHOCK

1) = Hpyovolemic Shock

2) = Cardiogenic Shock

3) = Anaphylactic Shock

4) = Neurogenic Shock =96 Vasovagal or = Psychogenic Shock

5) = Septic Shock =96 Hyper dynamic or Warm = Shock

6) = Traumatic Shock

7) = Burn Shock

Hpyovolemic=20 Shock

It is the most common = form of=20 shock seen in clinical practice. It is caused by depletion of = circulation blood=20 volume can be caused by loss of either whole blood or ultra filtered = plasma due=20 to increased vascular permeability as seen in peritonitis and burns.

Pathophysiology of=20 Hypovolemic Shock

Loss of varing amount of blood or any of its = constituents=20 result in decreased blood volume, which in turn leads to decreased = venous return=20 to heart. The decreased cardiac filling causes fall in stroke volume = which in=20 turn leads to fall in cardiac output and fall in arterial blood = pressure.

&n= bsp; =20 The fall in the blood pressure is sensed by the stretch receptors = present=20 in the carotids and the aortic arch which increases Sympatheto- adrenal=20 stimulation. In an effort to rise the blood pressure. This causes = increase in=20 heart rate to restore the cardiac output.

&n= bsp; =20 This causes increase sympathetic stimulation which causes = increase in the=20 heart rate and contractibility of myocardium. The fall in blood pressure = causes=20 hypoxia and change in pH of blood.

The hypoxia is predominantly sensed by the = peripheral=20 chemoreceptor present in carotid and aortic arch, while the change in pH = is=20 predominantly sensed by the central chemoreceptors present in medulla of = brain.=20 All these causes increased sympathetic activity. Heart rate is also = increased by=20 inhibition of the vagal fibres.

Increased sympathetic activity causes peripheral = vaso=20 constriction.The peripheral vaso contriction is more effective in the = blood=20 vessels of the skeletal muscles, than the blood vessels of heart and = brain.The=20 vaso contriction reduces the size of the vascular space.

&n= bsp;=20 There is also reduction of capillary hydrostatic pressure. The = reduced=20 capillary hydrostatic pressure encourages the fluid to move from the = extra=20 vascular space to the intra vascular space, thus trying to reduce the=20 hypovolemia and increased the blood pressure.

Other=20 mechanism that helps to maintain the normal circulation after=20 hypovolemia.

= ; =20 I. = Reduction of renal blood flow increases the production = of=20 enzyme rennin.

=20 II. = The rennin leads to formation of Angeotensin II which = is a=20 potent vasoconstrictor.

=20 III. = Release of aldosteron from the adrenal cortex which = increase=20 sodium reabsorption and fluid retention by the kidneys.

=20 IV. = Release of ADH by the posterior pituitary leads to = retention of=20 fluid by the kidneys.

When the blood loss is 25% or less the compensatory = mechanism=20 restores the blood pressure.

The vaso constriction of arterioles is more than = the venules,=20 so that hydrostatic pressure in capillary is low which increase the = movement of=20 fluid from extra celluler space to intra vascular compartment.

&n= bsp; =20 CARDIOGENIC SHOCK =96 Pump failure

Myocardial infarction causing more than 50% of wall = of left=20 ventricle. It is also seen in pulmonary embolism when there is a right = sided=20 heart failure.

AMPHYLACTIC=20 SHOCK

There is antigen antibody reaction. The antigen = combines with=20 the antibody present over surface of mast cell and basophils causing = release of=20 chemical substances e.g. histamine, SRSA-slow reacting substance of = anaphylaxis=20 leading to laryngeal edema, bronchospasm, respiratory distress and = hypoxia.=20 Beside this the histamine and SRSA causes massive peripheral = vasodilation and=20 hypovolemia shock.

NEUROGENIC=20 SHOCK &n= bsp; &nb= sp; =20

Also known as Vasovagal or Psychogenic = Shock. There=20 is fainting attack caused by intense pain or sudden fright. There is = sudden=20 paralysis of vasomotor influence, causing peripheral vasodilation and = fall of=20 peripheral vascular resistance and pooling of blood decreases venous = return to=20 heart. Decreased cardiac output and fall of B.P. which causes reflux = vagal=20 stimulation and bradycardia. Cerebral hypoxia causes unconsciousness. =

=20 Milder = form is=20 treated by removal of offending stimuli that is releaf of pain which = causes=20 rapid gain of vascular tone.

=20 Severe form is treated by IV fluids and vasopressure drugs which = causes=20 peripheral vasocontrition and increase of cardiac output.

SEPTIC=20 SHOCK-- HYPER DYNAMIC = OR WARM=20 SHOCK

Septic shock is caused by Gram Positive or Gram = Negative=20 bacterial infection. Septic shock is most commonly caused by Gram = Negative=20 bacteria. Gram positive bacterial infection can easily be controlled so = a septic=20 shock caused by gram positive bacterial infection is less dangerous.

Septic shock is mostly caused by the gram negative = bacterial=20 infection arising from=97genitourinary, pulmonary, hepatobiliary and=20 gastrointestinal tract.

Septic shock causes derangement of

F = Cardiac function

F = Capillary permeability

F = Vascular resistance

F = Cellular metabolism

Gram Negative bacterial infections causing Septic = shock=20 are=97

E.coli, klebsiella, proteus, pseudomonas and = bacteroids.

Enodotoxins are the constituents of bacterial call = wall,=20 which are released when the bacteria dies.

Enodoxin causes=97

1. = Release of kinens and histamine which are vaso active=20 peptides.

2. = Endothelial damage causing increased microvascular = permeability=20 resulting in fluid loss from intravascular spaceto extra vascular space. = Loss of=20 blood volume resulting in decreased venous filling, fall in CVP. Cardiac = output=20 falls resulting in hypotension. Hypotension is further aggrevated by = kinens,=20 histamines and other vasoactive peptides which causes peripheral vaso=20 dilation.

The endotoxin released by the bacteria causes = activation of=20 coagulation DIC. There is fall in coagulation factor and = platelets.Leading to=20 haemorrhage from various sites. There is upper GI, lower GI bleeding,=20 hematuria.etc.

The Septic Shock effects nearly all the organs = systems of the=20 body but the pulmonary, cardiovascular, renal and hepatic system are the = target=20 organs.

At first there is hyper dynamic state. There is = increased=20 cardiac output and trachecardia, warm and dry skin. The endothelium = becomes=20 damaged and endotoxins leaks into the circulation leading to a = generalised=20 inflammatory state.

TRAUMATIC=20 SHOCK

It is due to hypovolemia due to excessive external = or=20 internal bleeding. Trauma to the heart itself may cause pump=20 failure.

When the blood loss is 25% or less then = compensatory=20 mechanism restore the blood pressure to normal. When there is severe = internal=20 haemorrhage, Blood collecting into Pleural, peritoneal space, retro = peritoneal=20 and soft tissue blood collection, requires immediate surgical = intervention,=20 rather then to continue with fluid replacement.

BURN = SHOCK

When the burn is more than 25% of the body surface = area=20 leading to capillary leakage and hypovolemia. Later the septic shock = adds up and=20 worsens the condition.

MANAGEMENT=20 OF SHOCK

=A8 =20 HYPOVOLEMIC=20 SHOCK=97

Clinical Signs of Shock

(1) =20 Cold and sweating skin.

(2) =20 Pallor

(3) =20 Rapid pulse rate

(4) =20 Fall in blood pressure

(5) =20 Respiration is shallow and rapid

(6) =20 Level of consciousness in reduced

Sign of hypovolemic shock depends = on the=20 degree of hypovolemia

=D8 = Mild=20 hypovolemia -- = <20% of blood loss. There is = sign of=20 sympathetic discharge

=96 Cold and sweating skin = particularly of=20 lower limbs and feet.

=96 Increasing pulse rate =

=96 Blood pressure = falls.

=D8 = Moderate=20 hypovolemia=9720 to 40% of blood loss. The Compensatory = mechanism=20 to restore the blood pressure to normal starts. So reduce the = sign of=20 sympathetic discharge.

&n= bsp; &nb= sp; =20 =97 Urine output is low indicating the ADH release =

=96 Pulse = rate is=20 moderately elevated

=96 Blood = pressure may=20 be normal at lying down position

=D8 = Severe=20 Hypovolemia-- >40% of blood loss

=97 = ; =20 Signs of sympathetic discharge

=97 = ; =20 Increase pulse rate

=97 = ; =20 Blood pressure is low

=97 = ; =20 Decreased urinary output

=97 = ; =20 Cerebral ischemia leading to irritability and=20 confusion

PARAMETERS = INDICATING=20 CIRCULATORY COMPENSATION

1. = Level of=20 cerebral activity

2. =20 SpO₂ measurement

3. = Hourly=20 urine output it should be 30 to 50 ml per hour.

4. = CVP=20 measurement =96 normally it is 3=975 cms above the maniburosternal=20 angle.

5. = Swan=20 Ganz Catheter tracing =96 pulmonary artery and pulmonary capillary wedge = pressure=20 measurement.

Balloon tipped, = flow directed=20 Swan Ganz Catheter is useful in long term care of shocked patient. The = device is=20 not indicated in early management of shock because CVP measurement gives = quick=20 and easy information. The Swan Ganz catheter is introduced through the = internal=20 juglar vein into the right atrium and right ventricle and placed in the=20 pulmonary artery. The pulmonary artery and pulmonary capillary wedge = presuure=20 are measured. Swan Ganz catheter is ideal for monitoring volume = replacement in=20 injured patient with myocardial disease.

TREATEMENT OF = HYPOVOLEMIC=20 SHOCK

(1) = IV=20 fluid =96 A large bore IV line should be inserted or a venisection is = done.

=20 Initial resuscitation is done by crystalloids (Ringer lactate or = sodium=20 chloride) followed by colloids. Colloids are suitable to replace small = blood=20 loss. Among colloids Dextran is used=20 =96

(a) = Low=20 molecular weight dextran =96 has an immediate effect in replacing blood = volume but=20 their effect is short lasting as they are rapidly excreated by the=20 kidneys.

(b) High = molecular=20 weight dextran=97has a = delayed effect=20 in restoring blood volume, but their effect is long = lasting.

(2) = Volume=20 infusion is alone not enough to restore the arterial blood pressure and = tissue=20 perfusion, because of low peripheral vascular resistance. Then the use = of=20 cardiotonic and vasoactive drugs are used.

Dopamine =96 It improves the = cardiac=20 function and at the same time causes vaso dilatation of splanchnic and = renal=20 blood vessel and improves blood flow. A Dose of 1=975 mmg/kg/min is mild inotropic. = Successful=20 resuscitation is indicated by warm and dry skin indicating good tissue=20 perfusion. Rise in urinary output to 30 to 50 ml/hr.

Dobutamine=97improves the = cardiac=20 function but causes increase in the heart rate and decrease the = peripheral=20 vascular resistance.

(3)Use = of=20 steroids are controversial but it has been shown that = steroids.

=96 Improve = the cardiac=20 function

=96 Produce = mild=20 peripheral vasodilatation

=96 Protects = the=20 endothelial cells from endotoxins.

So a high = dose and a=20 short term use of steroids have no side effects and may be safely = recommended in=20 the management of shock.

(4)Positioning=97supine=20 position with limbs elevated

(5)Medical anti=20 shock trousers(MAST)

(6)Sedation-Given=20 IV to reduce pain and fright.

Treatment of = Septic=20 Shock

It must be = made clear=20 that an established case of septic shock is mostly fatal. So a prompt=20 recognition and Treatment of infection before septure shock develops is = the only=20 way to reduce mortality.

(1) = Patient=20 should be treated in ICU.

(2) = Direct=20 arterial blood pressure monitoring.

(3) = CVP=20 monitoring, pulmonary capillary wedge pressure monitoring, by Swan Ganz=20 Catheter.

(4) =20 Arterial and venous blood gas monitoring =

(5) = Urine=20 output measurement

(6) = Search=20 for source of infection and its treatment. If abscess is present then = its=20 drainage. If abdomen is the source of infection then Exploratory=20 Laparotomy.

(7) = Use of=20 antibiotics=97culture specimen is to be taken before starting = antibiotics. One=20 antibiotic may not be enough to cover all the organisms. Two antibiotics = are=20 used together once the culture report comes after 48 hr then a specific=20 antibiotic is started.

(8) =20 Maintenance of proper air way and O₂₌₂₀supplementation. If ARDS develops then the use of positive end = expiratory=20 pressure (PEEP) Ventilators are used.

Initial Signs of Gram Negative = Sepsis

(1) =20 Chills

(2) = Raised=20 body temperature-101^oF.

(3) =20 Hyperventilation-- Respiration is shallow and = rapid.=20 Mild degree of hypoxia causes hyperventilation and = alkalosis.

(4) =20 Oliguria

(5) = Altered=20 Sensorium

(6) = White=20 blood cells are raised except in patients very ill patient and those = receiving=20 immuno suppressant.

(7) = Fall of=20 platelet count may be early and sensitive indicator of gram negative=20 sepsis.

=20 Clinical signs of septic shock depend on the previous volume = status of=20 the patient.

So a=20 septic shock can present as

= =96=20 Hyper dynamic septic shock

=96 Hypo = dynamic septic=20 shock

HYPER DYNAMIC=20 SEPTIC SHOCK=97

In hyper = dynamic septic=20 shock the previous volume status of patient (i.e.before sepsis starts) = is normal=20 e.g. septic abortion.

There is =96

(a) =20 Hyper = ventilation=20 (respiration is shallow and rapid)

(b) High = CVP

(d) =20 Alkalosis

(e) = Oliguria=20

(f) =20 Low peripheral resistance

(g) = Low=20 blood pressure

(h) = Warm and=20 dry skin

Aim of = treatment is to=20

= ; = =20 i. = ;=20 Further increase of cardiac output

= ; = =20 ii. = ;=20 Antibiotic therapy

= ; = =20 iii. = ;=20 Early surgical intervension

If the = control of=20 infection is delayed patient passes into acidotic phase fall in cardiac = output=20 and further cellular damage. This may not respond to = treatment.

HYPODYNAMIC=20 SEPTIC SHOCK =96

=20 Is seen in patient who are already = hypovolemic=20 or the volume status of the patient is low before the septic process = starts.=20 E.g. Gangrenous intestinal, obstruction, mesenteric artery thrombosis,=20 peritonitis. There is third space fluid loss.

They present = with=20 =96

1. = Low CVP

2. = Low cardiac output

3. = Low blood pressure

4. = Oliguria

5. = Increased peripheral resistance

6. = Cold and synoptic limbs