MANAGEMENT OF

SHOCK

SuamePrecious

OBJECTIVES

Define shock and its different categories.

Review basic physiologic aspects of shock.

Describe the management of shock.

Definition of ShockShock is an abnormal physiological state resulting

from wide-spread and serious reduction of tissue perfusion that if prolonged will lead to generalized impairment of cellular function.

Inadequate tissue perfusion to meet tissue demands

Usually as a result of inadequate blood flow and/or oxygen delivery.

Classification and Causes of Shock(1) HYPOVOLEMIC SHOCK (DECREASE IN BLOOD

VOLUME):Hemorrhagic

Cutaneous shock: burns

(external fluid loss)

Gastrointestinal

(vomiting&diarrhea)

Diabetic shock

Diabetes insipidus.

Excessive use of diuretics.

Internal sequestration

(fractures,

hemothorax,ascites)

2) CARDIOGENIC (DECREASED CARDIAC OUTPUT)

Myocardial infarction

Arrhythmias

Pump failure

(3) DISTRIBUTIVE/NEUROGENIC SHOCK:

Sepsis

Anaphylactic

-Insulin shock

-Barbiturate injection

-Anaesthesia (spinal)

Spinal cord injury

(4) OBSTRUCTIVE

Massive Pulmonary

embolism

Tension pneumothorax

Cardiac tamponade

Constrictive pericarditis

Aortic stenosis.

Classification according to degree: Compensated: Organ perfusion is maintained.

Uncompensated: Circulatory failure with end

organ dysfunction.

Irreversible: Irreparable loss of essential

organs.

CLINICAL ALTERATIONS IN SHOCKRestlessness.

Apathy & confusion.

Unconsciousness.

Rapid thready pulse

followed by weak

pulse.

Increased respiratory

rate, shallow

respiration.

Decreased BP

Subnormal

temperature

Cold & clammy skin

Decreased urinary output

Cyanosis

Decreased/absence

bowel sound

PATHOPHYSIOLOGY

Initial stage

Compensatory stage

Progressive stage

Refractory stage

Initial stage

• Hypo-perfusion leads to hypoxia.

• lactic acid begins to accumulate,

leading to lactic acidosis.

compensatory stage Physiologic response to hypovolemia is directed at preservation of

perfusion to vital organs.

Stimulation of renin angiotensin system in order to increase cardiac contractility & peripheral vascular tone Release of Anti-Diuretic Hormone (ADH) to conserve salt and water. Change in local micro circulation to regulate regional blood flow.

Victim begins to Hyperventilate

Mediation via Baro & chemo receptors which stimulates ANS & HPA axis to Release of epinephrine & norepinephrine.

Compensatory (Hormonal response)

HyperglycemiaLypolysisGluconeogenesisGlycogenolysis

Cortisol

ACTH

CRH

HYPOTHALAMUS

Progressive stage

•Compensatory mechanism begins to fail.

•Anaerobic metabolism progresses, increasing metabolic acidosis.

Refractory stage

•There is organ failure.

•Shock is irreversible.

•Brain damages and cells die.

•Death occurs imminently.

MANAGEMENT OF SHOCK:GENERAL Principles of shock management

The overall goal of shock management is to improve oxygen delivery/utilization in order to prevent cellular and organ injury.

Effective therapy requires treatment of the underlying etiology.

Restoration of adequate perfusion, monitoring and comprehensive supportive care.

Interventions to restore perfusion center on achieving an adequate B.P increasing cardiac output and optimizing oxygen content of the blood

Oxygen demand should also be reduced.

Initial Treatment in Shock-Assess airway and breathing Airway and begin CPR if necessary.

-Lay the person down.

-Elevate feet unless head, neck, hip or leg is injured.

-Turn patient to his side if vomiting or bleeding from the mouth.

-Keep patient warm.

-Administer oxygen if available.

-Treat obvious injuries.

-Administer volume expansions (usually Normal Saline).

Restoration of CirculationVOLUME- FLUID CHOICES:

CRYSTALLOIDS VS COLLOIDS

Crystalloids: for initial resuscitation

IVF 0.9% Normal Saline is the fluid of choice. Give 2-3 liters over 15-30 min.

Ringers lactate may also be used.

Colloids: to replace blood lossAlbumin

Dextran

Blood

•They are great volume expanders used for major haemorrhage

DIAGNOSTIC INVESTIGATIONS

Blood test

• Fasting Blood Sugar (FBS)

• Random Blood Sugar (RBS)

• Microscopic Culture and Sensitivity test (MCS)

X- ray

Electrocardiogram (ECG)

Echocardiogram (ECHO)

Pulmonary artery catheterization

DRUGS USED IN SHOCK MANAGEMENT

Inotropes –cardiac support

Vasopressins (pitressin)

Steroids

InotropesAgent Site of Action Dose

Mcg/kg/min

Effects

Dopamine Dopaminergic

Beta

Alpha < Beta

1-3

5-10

11-20

Renal vasodilation

Inotrope/vasoconstriction in order to increase BP

Increase peripheral. Vascular resistance

Dobutamine Beta 1 & 2 1-20 Inotrope

Vasodilation

Epineprhine Beta < alpha 0.05 – 1.0 Inotrope, vasoconstriction

Tachycardia

Norepinephrine Alpha < beta 0.05 – 1.0 Profound vasoconstriction

inotrope

Nitroprusside Vasodilator

(arterial < venous)

0.5 – 1.0 Vasodilation

Milranone Phosphodiesterase inhibitor 0.5 – 0.75 Inotrope

vasodilation

Vasopressin (pitressin)

Initiates reabsorption of water by the kidney

Also causes constriction of blood vessels.

Blood flow diversion from non-vital to vital

organs

Dosage 0.01 – 0.04U/min up to 0.08U/min IV

Steroids

Glucocorticoid function

-Maintain homeostasis.

-Increases BP.

-Modulate inflammatory response.

-Normalize vascular reactivity.

-Boosts blood glucose level.

Dosage: Hydrocortisone 200 mg IV

Hypovolemic shock• It occur when the intra vascular volume is depleted relative to

the vascular capacity.

Mild (<20%) Moderate(20-40%) Severe(<40%)

-Cold

extremities

-Decreased CRT

-Diaphoresis

-Anxiety

Same +

-Tachycardia

-Tachypnoea

-Oliguria

-Postural

hypotension

Same +

-Hypotension

-Mental status

deterioration

MANAGEMENT OF Hypovolemic shock

I.V. fluid normal saline 2-3 liters over 15-30 min.

If hemodynamic instability persist then start blood transfusion & control on going heamorrhage.

Give Inotropes:

Dopamine 5-10microgms/Kg/min

Dobutamine 2-20microgms/Kg/min

Cardiogenic shock• Circulatory pump failure • Sustained hypotension SBP < 90 mm

Hg for at least 30 minutes.

MANIFESTATIONS

• Chest pain

• Hypotension

• Arrhythmias

MANAGEMENT:

Conformation of diagnosis by ECG, ECHO & X-RAY.

Intubation & mechanical ventilation often required.

Avoid fluid overload.

Inotropic support preferably Dobutamine 2-20microgms/Kg/min.

USG guided pericardiocentesis.

Neurogenic shock• DECRESED tissue perfusion as a

result of loss of vasomotor tone to peripheral arterial beds

• Secondary to spinal cord injury from vertebral

• Hypotension with bradycardia

• Warm extremities

• Motor and sensory deficit

MANAGEMENT

• Restoration of intravascular volume by crystalloids

• Administer vasoconstrictors:

Dopamine <10mcg/kg/min

OBSTRUCTIVE SHOCK• Blood flow is stopped as a

result of cardiac (or pericardiac) tamponade (the build-up of fluid in the pericardium) that compresses the heart and stops it from beating properly , or pulmonary embolism ( a blood clot in the pulmonary artery, blocking the flow of blood to the lungs)

MANAGEMENT

• Removing the obstruction , for example,surgery or clot-dissolving medication (heparin 3000-5000units IV) to remove a clot in the pulmonary artery.

Septic shock-Manifestation of excessive &

inflammatory response of endogenous immune mechanism

MANAGEMENT

Culture of body fluids

Infuse BSS 500 cc/15min monitor SBP/CVP

If hemodynamic instability persists start vasopressor preferably Norepinephrine 0.02-0.25microgms/Kg/min

Administer broad spectrum antibiotic

Case scenario1) A 25 year old trainee with no prior history of any chronic disease

presented to the emergency clinic complaining of weakness and had been stooling for the past 24 hours.

Temp:35.80C, pulse:129b/min, R.R: 27c/min, BP:100/58mmHgWhile still in the clinic, he rushed to the toilet. Coming out from the

toilet, he was restless, and showing apathy. Again V/S quickly recordedBP:95/56mmHg, PR:49b/min (weak), RR: 27c/min, and patient is

becoming more disoriented as V/S been checked.• a) What information do you need to determine if this client is in shock?• b) what would be your goal of management for this client?• c) What initial interventions are needed to stabilize that Pt.?

2) A 50 year old trainer (a known diabetic) was rushed into the emergency clinic with a history of sudden collapse while in the workshop.

On examination, he is unresponsive.

BP:110/60mmHg, pulse:67c/m, RR: 30b/m, temp: 36.9OC

• How can you ascertain that the client is in shock?

• What type of shock is he in if:

RBS is 25mg/dl

RBS is 358mg/dl

c) What are the probable etiologies of each type of shock

d) How will you manage this client?

CONCLUSION

Early recognition of warning signs and diagnosis in the initial stage is important for successful management of shock.

Hypovolemia and sepsis account for majority of shock.

Principles of initial resuscitation same irrespective of type of shock.

Ultimate treatment of underlying cause forms cornerstone of management.

Abbreviations

HPA----Hypothalamic Pituitary

Adrenal

CRH----Corticotropin-Releasing

Hormone

ACTH---AdrenoCorticotropic

Hormone

ADH----Anti Diuretic Hormone

ATP-----Adenosine TriPhosphate

BP ------Blood Pressure

CRT-----Capillary Refill Time

SBP-----Systolic Blood Pressure

ECG-----Electrocardiogram

ECHO---Echocardiogram

USG-----Ultrasonography

SIRS ----Sepsis Inflammatory

Response Syndrome

BSS------Balanced Salt Solution (eg

Ringers Lactate )

CVP-----Cell Volume Profile