SHOCK

Presented by
Dr.A.S.M Ariful Islam
Assistant professor & Head
Dept. of Oral & Maxillofacial Surgery
Update Dental College & Hospital
Definition-
Shock can be defined as a condition in which tissue
perfusion is inadequate to deliver oxygen and nutrients to
support vital organs and cellular function. OR
Shock is a syndrome characterized by decreased tissue
perfusion and impaired cellular metabolism.This results in
an imbalance between the supply of and demand of oxygen
and nutrients.
Causes
 Severe or extension injuries
 Severe burns
 Severe pain:heart attack/cardiac arrest
 Electric shock
 Loss of blood
 Exposure to extreme heat and cold
 Poison taken internally
 Bites of poisonous snake or insects
Pathophysiology
Switch from aerobic to anaerobic metabolism

Lactic acid production

Cell function ceases and swells

Membrane becomes more permeable

Electrolytes and fluids seep in and out of cell

Na+/K+ pump impaired

Mitochondria damage

Cell death
Stages of shock
Initial stage-
tissues are under perfused,decreased co2,increased anaerobic
metabolism,lactic acid is building.
Compensatory stage-
reversible,SNS activated by low CO,attempting to compensate for the
decrease tissue perfusion.
Progressive stage-
failing compensatory mechanisms:profound vasoconstriction from the SNS
ischemia lactic acid production is high metabolic acidosis.
Irreversible or refractory stage-
cellular necrosis and multiple organ dysfunction syndrome may occur.
Death is imminent
clinical presentation of generalized shock

Vital sign
• Hypotensive : < 90 mmHg.
• Tachycardia : weak and rapid thready pulse.
• Tachypneic : increased respiratory rate.
• Respiratory alkalosis.

Mental status
restless,irritable,apprehensive,unresponsive.
Decreased urine output.
Classification
I. Hypovolemic shock-blood volume problem
II. Cardiogenic shock-blood pump problem
III. Distributive shock -blood vessel problem
-septic shock
-anaphylactic shock
-neurogenic shock
Hypovolemic shock
Loss of circulating volume “empty tank’ decrease tissue perfusion
general shock response.
Etiology
Internal or external loss of fluid from intracellular and extracellular
compartments.
Most common cause-
 Hemorrhage.
 Dehydration.
 External loss of fluid:-

Nausea,vomiting,diarrhea,massive diuresis,extensive burns.

Internal fluid loss-
 Loss of intravascular integrity
 Increased capillary membrane permeability
 Decreased colloidal osmotic pressure
(third spacing)
Pathophysiology of hypovolemic shock
 Decreased intravascular volume leads to-
-decreased venous return(preload,RAP) leads to
-decreased ventricular filling(preload,PAWP) leads to
-decreased stroke volume(HR,preload and afterload) leads to
-decreased CO leads to (compensatory mechanism)
-inadequate tissue perfusion
Clinical presentation of hypovolemic shock

 Tachycardia and tachypnea

 Weak, rapid thready pulse
 Hypotension
 Cold and clammy skin.
 Mental status changes.
 Decreased urine output: dark and concentrated
Initial management of hypovolemic shock
Management goal: restore circulating volume,tissue
perfusion and correct the cause

 Early recognition( do not relay on BP!(30% fluid loss)

 Control hemorrhage
 Restore circulating volume
 Optimize oxygen delivery
 Vasoconstrictor if BP still low after volume loading.
Cardiogenic shock
 Due to cardiac pump failure related to loss of myocardial
contractility myocardium or structural failure of the cardiac
anatomy and characterized by elevations of diastolic filling
pressures and volumes.
 Cardiogenic shock occurs whenever the heart is unable to
pump as much as blood as the body needs.
 The most common causes are serious heart
complications.many of these occur during or after a heart
attack( myocardial infraction).
 Etiologies of cardiogenic shock
 Mechanical-
-papillary muscle rupture
-ventricular aneurysm
-ventricular septal rupture
 other causes-
-cardiomyopathies
-temponade
-tension pneumothorax
-arrhythmias
-valve disease
 Clinical presentation of cardiogenic shock
i. Chest pain or pressure
ii. Coma
iii. Decreased urination
iv. Fast breathing
v. Fast pulse
vi. Heavy sweating (moist skin)
vii. Light headedness
viii. Loss of alertness and ability to concentrate
ix. Restlessness,agitation,confusion
x. Shortness of breath
xi. Skin that feels cool to the touch
xii. Pale skin colour
xiii. Weak/thready pulse
xiv. dysarrythmea
Cont.
• Pulmonary and peripheral edema
• Hypotension
• Tachypnea
• JVD
• Co
• Uo
 Management
 Goal of management-
a) Treat reversible cause
b) Improve tissue perfusion
c) Early assessment and treatment
d) Protect ischemic myocardium
e) Optimizing pump by-
-increasing myocardial o2 delivery
-maximizing co
-decreased lv workload(after load)
 Limiting or reducing myocardial damage myocardial infarction:
 Increase pumping action & decrease workload of the heart-
-Inotropic agent
-vasoactive drugs
-cautious administration of fluids
-transplantation
o Consider thrombolytics,angioplasty
 Optimizing pump action
 Pulmonary artery monitoring is a necessary!
- aggressive airway management-mechanical ventilation
- judicious fluid management
- vasoactive agents-
dobutamine
dopamine
-morphine as needed(decreased preload,anxiety)cautious use of
diuretics in CHF
- vasodilator is needed for after load reduction
Distributive shock
 Inadequate perfusion of tissue through maldistribution of blood
flow
 Intravascular volume is maldistributed because of alteration in
blood vessels
 Cardiac pump and blood volume is normal but blood is not reaching
the tissues.
 Distributive shock including-
-septic shock(most common)
-anaphylactic shock
-neurogenic shock
 Septic shock
 Sepsis
systemic inflammatory response (SIRS) to infection manifested by :
-temp >38 or < 36 centigrade
-HR >90
-RR > 20 or paco2 <32
-WBC >12000 /cu mm or < 4000
>10% bands ( immature WBC)
Sepsis syndrome-
SIRS with cofirmed infectious process associated with organ failure or
hypotension.
Septic shock
 Risk factors associated with septic shock:
-Age
- Malnutrition
-General debilitation
-Use of invasive catheter
-Traumatic wound
-Drug therapy
pathophysiology
 Initiated by gram-negative (most common) or gram positive
bacteria, fungi, or viruses.
 Cell wall of organisms contains endotoxins
 Endotoxins release inflammatory mediators

which causes-
vasodialation & increase capillary permeability leads to
shock due to alteration in peripheral circulation & massive
dilation.
... Injury or infection

Local inflammatory reaction

Release of mediators

Systemic inflammatory response

Difuse endothelial injury,vasodialation and increased capillary permeablity

Progressive vasodilatation and maldistribution of blood flow

Organ hypoperfusion

Multiple organ dysfunction syndrome

 Clinical presentation of septic shock-
 Early hyperdynamic state- (compansation)
 pink,warm,flushed skin
 Increased heart rate
 Tachypnea
 Massive vasodilation
 Increased co
 Crackles
-Late hypodynamic state- ( decompansation)
 Vasoconstriction
 Skin is pale and cold
 Tachycardia
 Decrease bp
 Management
 Prevention
 Find and eradicate the source of the infection
 Fluid resuscitation
 Vasoconstrictors
 Inotropic drugs
 Maximize oxygen delivery support
 Nutritional support
 Comfort and emotional support
Anaphylactic shock

 A type of distributive shock that results from widespread

systemic allergic reaction to an antigen.
 This hypersensitive reaction is life threatening.
 Pathophysiology of anaphylactic shock
 Antigen exposure
 Body stimulated to produce lgE antibodies specific to antigen
-drugs,bites,contrast,blood,foods,vaccines
 Reexposure to antigen
-IgE binds to mast cells and besophils
 Anaphylactic response-
 Vasodilatation
 Increased vascular permeability
 Bronchoconstriction
 Increase mucus production
 Increased inflammatory mediators to sites of antigen interaction.
 Clinical presentation of anaphylactic shock
 Almost immediate response to inciting antigen
 Cutaneous menifestations
-urticaria,erythema,pruritis,angioedema
 Respiratory compromise
-stridor,wheezing,bronchorrhea,resp.distress
 Circulatory collapse
-tachycardia,vasodilation,hypotension.
Management

 Early recognition,treat aggressively

 Airway support
 IV epinephrine (open airway)
 Anti-histamine
 Corticosteroids
 Immediate withdrawal of antigen if possible
 prevention
 Neurogenic shock
 A type of distributive shock that results from the loss or suppression of sympathetic
tone.
 Causes massive vasodilatation in the venus vasculature,venous return to heart,cardiac
output.
 Most common etiology: spinal cord injury above T6,syncope of fainting
 Neurogenic is the rarest form of shock!
Pathophysiology
Disruption of sympathetic nervous system

Loss of sympathetic tone

Venous and arterial vasodilation

Decreased venous return

Decreased stroke volume

Decreased cardiac output

Decreased cellular oxygen supply

Impaired tissue perfusion

Impaired cellular metabolism

 Clinical features of neurogenic shock
 Hypotension.
 Bradycardia.
 Hypothermia.
 Warm, dry skin.
 CO.
 Flaccid paralysis below level of the spinal lesion
 Medical management
 Goals of therapy are to treat or remove the cause & prevent cardiovascular instability
& promote optimal tissue perfusion.
 Hypovolemic-Rx with careful fluid replacement for BP< 90 mmhg.
 Observe closely for fluid overload.
 Vasopressors may be needed.
 Hypothermia-warming avoid large swings in patients body temp.
 Treat hypoxia.
 Cont....
 Maintain ventilatory support-
-alpha agonist to augment tone if perfusion still inadequate
-dopamine.
-ephedrine.
-treat bradycardia with atropine 0.5 -1 mg doses to maximum 3 mg. May need
transcutaneous or transvenous pacing temporarily.