"Shock" is a multifaceted condition that can range from being mild to extremely fatal. This is a condition whose knowledge is a must for medical practitioners; especially the one in the field of Dentistry.

1. SHOCK & ITS
MANAGEMENT
Dr. Balraj Shukla
Department of Pedodontics & Preventive Dentistry
College of Dental Sciences & Research Centre

2. CONTENTS
SHOCK
DEFINING SHOCK
CELLULAR METABOLISM
STAGES OF SHOCK
HAEMODYNAMIC
FACTORS
SEVERITY OF SHOCK
HYPOVOLAEMIC SHOCK
CARDIOGENIC SHOCK
SEPTIC SHOCK
ANAPHYLACTIC SHOCK
NEUROGENIC SHOCK
DISSOCIATIVE SHOCK
MANAGEMENT
DIFFERENTIATING SHOCK
INITIAL MANAGEMENT
GOALS OF THERAPY
FIRST HOUR OF
RESUSCITATION
VOLUME RESUSCITATION
DRUGS USED
ANAPHYLAXIS - CHAIRSIDE
CONCLUSION
REFERENCES

3. DEFINING SHOCK
• “Shock is a loosely defined term used to describe the clinical
syndrome that develops when there is critical impairment of
tissue perfusion due to some sort of acute circulatory failure.”
– Davidson’s Principles and Practice of Medicine
• “Shock is an acute syndrome in which the circulatory system
is unable to provide adequate oxygen and nutrients to meet
the metabolic demands of vital organs.”
– Textbook of Pediatric Emergency Medicine

4. CELLULAR METABOLISM
• Aerobic metabolism
- Kreb’s Cycle: O2 + Glucose = ATP
- Adequate blood flow & patent airway
• Anaerobic metabolism
- Uses stored glucose in the form of glycogen for energy
production
- Increased lactic acid as a by-product
- Energy supplied for a short period of time

5. OXYGENATION
• The body’s ability to facilitate the supply of oxygen to all the cells through
various mechanisms is called oxygenation.
- Respiration
- Diffusion
- Perfusion

6. FACTORS AFFECTING PERFUSION
• Rate of oxygen delivery
• O2-Hb Dissociation
• Size of capillary to cellular pO2
• Diffusion distance from capillaries to the cells
• Rate of O2 utilized in cellular metabolism
PaO2 level (mmHg) Clinical Signs
80-100 Normal
55-60 Short term memory loss, Euphoria, Impaired Judgement
30-50 Progressive loss of motor and cognitive functions, tachycardia
<30 Loss of consciousness

7. • Hypoperfusion
• Hyperperfusion
• Overperfusion
• Underperfusion
• Ischemia
• Reperfusion injury
TYPES OF MALPERFUSION

8. TOLERANCE TO HYPOPERFUSION
* Leach RM, Treacher DF. Oxygen transport-2. Tissue hypoxia. BMJ. 1998;317(7169):1370–
1373.
Tissue Survival time
Brain <3 min
Kidney and liver 15-20 min
Skeletal muscle 60-90 min
Vascular smooth muscle 24-72 h
Hair and nails Several days

9. NON-PROGRESSIVE
SHOCK
STAGES OF SHOCK
MILD to MODERATE / PROGRESSIVE
SHOCK
IRREVERSIBLE / SEVERE
COMPENSATED
DECOMPENSATED

10. NON-PROGRESSIVE / COMPENSATED SHOCK
1. Baroreceptor reflex & Central Nervous System Ischemic Response
2. Reverse Stress-Relaxation of Circulatory system
3. Release of Renin & Angiotensin II
4. Increased secretion of Vasopressin by Pituitary Gland
5. Epinephrine & Norepinephrine secretion by adrenal medulla
Re-adjustment of blood volume: 1 - 48 hours

11. Hypoperfusion IschemiaAnaemia Hypoxia
Mitochondrial dysfunction
Hypothermia Low pH
Metabolic AcidosisVasoconstriction
Decreased
hydrostatic pressure
Debris Accumulates
Thrombi
Coagulopathy
Release of
lysosomal
enzymes
Cell membrane dysfunction
Sodium pump fails
Sodium &
Water enter the
tissues
Oedema
Cellular death
Organ death
Shock & the Cascade of
Death
DECOMPENSATED / PROGRESSIVE SHOCK

12. SEVERE / IRREVERSIBLE SHOCK
Depletion of cellular high-energy phosphate reserves
• Creatinine Phosphate  Degrades
• ATP  ADP  AMP  Adenosine  Enters circulating blood & is
converted to Uric Acid  Even more acidosis

13. HAEMODYNAMIC FACTORS IN SHOCK
• Perfusion
• Cardiac Output
• Stroke Volume
• Preload
• Afterload
• Contractility
• Systemic Vascular Resistance
• Mean Arterial Pressure
• Venous return/ Central Venous Pressure

14. SEVERITY OF SHOCK
MILD: <20% Blood loss, Cool & Pale Extremities, Sweating, Thirst
MODERATE: 20-40% Blood loss, Oliguria, Pulse is <100
SEVERE : >40% Blood loss, Pallor in extremities

15. TYPES OF SHOCK
• Hypovolaemic
• Cardiogenic & Obstructive shock
• Distributive (Sepsis, Anaphylaxis, Neurogenic)
• Dissociative

16. HYPOVOLAEMIC SHOCK
• Sudden loss of blood volume or loss of fluid from vascular
space
Haemorrhagic
Internal Bleeding
Trauma
Severe Haemoptysis
Ectopic pregnancy
Non-Haemorrhagic
Bowel Obstruction
Burns
Dehydration (Vomiting,
Diarrhoea, Excessive
Sweating)

17. CLASSIFICATION OF
HAEMORRHAGIC SHOCK

18. PATHOPHYSIOLOGY OF HYPOVOLEMIC SHOCK DUE TO
HAEMORRHAGE
Haemorrhage from small veins & venules (50%)
Decreased filling of the right heart
Decreased filling of pulmonary vasculature
Decreased filling of left ventricle & atrium
Decrease of ventricular stroke volume
Drop in arterial blood pressure
Poor perfusion to pulmonary arteries
Cardiac dysfunction & pump failure

19. BOWEL
OBSTRUCTION
PATHOPHYSIOLOGY OF HYPOVOLEMIC SHOCK DUE TO
NON-HAEMORRHAGIC CONDITIONS
Intestinal Obstruction
Blockage of venous blood flow
Increase in intestinal
capillary pressure
Fluid containing high
amount of protein leaks in
intestinal walls
Reduced blood plasma volume

20. BURN
SHOC
K
BURN
Increased vascular
permeability
Rapid plasma loss from
damaged tissues
Intravascular
inflammatory
response
Decreased
cardiac output
Hypovolemic
shock

21. HYPOVOLAEMIC SHOCK IN CHILDREN
• Diarrhoea is the most common etiology for hypovolaemic
shock in children (WHO).
• Amount of fluid loss required to produce shock in a child is
less compared to adults.
• Tachycardia is the most common compensatory mechanism in
children suffering from hypovolaemic shock.
• C/F: Sunken eyes, sunken fontanelle, cool extremities,
prolonged capillary refill, hypotension (after 30% fluid loss)

22. CARDIOGENIC SHOCK
• Due to dysfunction of ventricles of the heart
• Caused due to myocardial infarction, chronic congestive heart
failure, cardiac arrhythmias, pulmonary embolism or systemic
arterial hypertension
• Cardiac compressive shock: External compression of the heart to
an extent that the cardiac output is decreased. Caused due to
tension pneumothorax, pericardial tamponade, aortic stenosis or
pulmonary embolism.
RIGHT VENTRICULAR
DYSFUNCTION
Decrease in blood flow to the lungs
Distended neck veins
Enlarged liver
LEFT VENTRICULAR DYSFUNCTIO
Abnormal third heart sound
Distended neck veins
Bronchial rales

23. CLASSIFICATION

24. CLINICAL FEATURES
(COMMON TO BOTH CHILDREN & ADULTS)
• Thready pulse
• Cool extremities
• Hepatomegaly
• Periorbital oedema
• Pulmonary oedema
• Low urine output
• Decreased blood pressure

25. THE SEPTIC SPECTRUM
SIRS
• Temperature is >38.5◦C or <36◦C
• HR >90
• RR>20 or PaCO2 <32
• WBC count >12,000 or <4,000
Sepsis
• SIRS + Confirmed infection
• Severe sepsis: Sepsis + 2 or more organ dysfunction
Shock
• Sepsis + Irreversible cardiovascular dysfunction
• Most common cardiovascular dysfunction: Hypotension
MODS
• Organ failure

26. SEPTIC SHOCK
Antigens enter the bloodstream & interstitial
tissue
WBCs attack the antigens within the bloodstream & release
NO2
Vasodilatation + Increased permeability of blood vessels
Interstitial fluid leaked out accumulates & doesn’t allow the RBCs to transport
oxygen to the peripheral tissues
Lytic enzymes released from WBCs destroy the blood vessels
Coagulation system activated
Coagulation factors are used up
Clots formed in the
blood vessel break off
Subsequent breakage of vessel
wall causes the blood to spill out
Cardiac Output, the lone compensatory mechanism, fails
Decrease in blood pressure
Sympathetic system causes vasoconstriction
Cold skin

27. CLINICAL FEATURES
• Gram +ve infection:
- Clostridium,
Staphylococcus,
Streptococcus or
Pneumococcus groups
- Massive fluid losses
- No reduction in cardiac
output
- Progressive hypotension
- Normal urine output
• Gram -ve infection:
- E.Coli, Klebsiella,
Pseudomonas, Proteus groups
- Caused in areas where
previous operations/
instrumentations have been
carried out.
- Genitourinary tract,
Respiratory tract & GIT
most commonly infected
- Poor prognosis

28. Goldstein B et al,
Pediatr Crit.
Care Med. 6, 2-8

29. PEDIATRIC SEPTIC SHOCK
• SIRS cannot be diagnosed in children in absence of changes in leukocyte
counts or temperature.
• Bradycardia can be used as evidence for SIRS in newborns (0 to 1 week).
• Pediatric Logistic Organ Dysfunction Syndrome (PELOD) is the most
commonly used scale to assess the severity of MODS in children.
• Children with MODS have a worse prognosis irrespective of the diagnostic
category of sepsis.
• In children, MODS occurs only when there is an underlying primary or
secondary immunodeficiency.
• Infections caused in sepsis are primarily due to Staphylococcus,
Streptococcus & E.Coli which target the respiratory tract. Fungal
infections are the second most common etiology for septic shock in
children.
• Low-birth-weight infants are most vulnerable to septic shock.
• Prevalence of severe sepsis is more in boys compared to girls

30. ANAPHYLACTIC SHOCK

31. Histamine, Bradykinin & Leukotrienes released by mast cells
Vasodilatation
Venous return &
CO decreases
Tissue perfusion
decreases
Hypotension
Increased permeability of
blood vessels
Increased accumulation of
fluid in interstitial space
Oedema
AngioedemaStridor
Decreased O2 supply
Shock

32. CRITERIA TO CONFIRM ANAPHLAXIS
Anaphylaxis is highly likely when any 1 of the 3 criteria are fulfilled:
• Acute onset of an illness (minutes to several hours):
- Skin & Mucosal involvement with Respiratory compromise/Reduced
BP/End-organ dysfunction
• Reduced blood pressure after exposure to allergen (minutes to hours):
- Infants & children: Low systolic BP which is age specific
• 2 of the following 4 criteria (minutes to several hours):
- Skin-Mucosa involvement
- Respiratory distress
- Hypotension/End-organ dysfunction
- Persistent GIT distress
AGE SYSTOLIC BP
1 month – 1 year 70 mmHg
1 – 10 years [70 mmHg +
(2*current age)]
11-17 years 90 mmHg

33. NEUROGENIC SHOCK
Injury to nervous system
Loss of sympathetic tone
Persistent vasodilatation of blood vessels make them floppy
Decreased SVR
Decreased O2 delivery Decreased venous return
Decreased tissue perfusion
Decreased BP
Decreased stroke volume
Decreased heart rate
Bradycardia
Shock
• Loss of vascular sympathetic tone and pooling of peripheral blood
because of an injury to the nervous system results in neurogenic
shock.
• In children, trauma to the spinal cord is the most common etiology.
• Bradycardia, Warm skin & decreased urine output are the most
commonly seen features in neurogenic shock.

34. DISSOCIATIVE SHOCK
• Dissociative shock is the type of shock wherein the haemoglobin molecule
fails to deliver oxygen to the tissues in presence of adequate tissue
perfusion.
HbO2 Tissue
s
binds with delivers O2

35. WHAT CAUSES THE LEFT SHIFT?
1) Methemoglobinemia: Presence of methaemoglobin (oxidized form of Hb)
in the blood
- Caused due to nitrates, pesticides, medications like trimethoprim,
dapsone, prilocaine and benzocaine.
4 Ferrous (Fe2+) groups
constitute a Hb molecule
One Ferrous ion is oxidized
to Ferric ion (Fe3+) where
O2 does not bind
Increased binding of the
O2 onto the other sites
Decreased tissue perfusion
Symptoms:
- Dizziness
- Headache
- Fatigue
- Dyspnoea

36. WHAT CAUSES THE LEFT SHIFT?
2) Carbon Monoxide Poisoning
- Binding efficiency of CO to Hb is 100 times greater than that of O2.
- No room for O2 binding and hence decreased oxygen delivery.
- Symptoms similar to that of methemoglobinemia.
- Caused due to smoke released from wood stoves, combustion engines, etc.

37. PEDIATRIC DISSOCIATIVE SHOCK
• Least common form of shock in paediatric individuals.
• Newborns under 4 months of age are most vulnerable to
dissociative shock.
• Newborns lack an enzyme known as Cytochrome B5 Reductase
which is responsible for conversion of Ferric ion to Ferrous ion,
thereby stabilizing the oxygen delivery through Hb.
• This enzyme becomes active in the body only after the first four
months of life.

38. MANAGEMENT OF SHOCK

39. HOW TO
DIFFERENTIATE
SHOCK ?

40. INITIAL MANAGEMENT OF
SHOCK

43. GOALS OF THERAPY
CLINICAL
• Urine output
>1ml/kg/hr
• Normal mental
status
• Capillary refill <2
seconds
HAEMODYNAMIC
• Normal blood
pressure
• Normal heart
rate
• Normal tissue
perfusion
BIOCHEMICAL
• Lactic acid level
<2mmol/L
• Anion Gap
<16mmol/L

44. FIRST HOUR OF
RESUSCITATION

45. Methods
This study was sponsored by the American Association for the Surgery of Trauma
multi-center trials committee. We performed a retrospective analysis of all patients
that presented to trauma centres with presumptive hypovolemic shock indicated by
pre-hospital or emergency department hypotension and need for intubation from
January 1, 2014 to July 1, 2016. Data collected included demographics, timing of
intubation, vital signs before and after intubation, timing of the blood transfusion
initiation related to intubation, and outcomes.
Results
From 440 patients that met inclusion criteria, 245 (55.7%) received intravenous
blood product resuscitation first (CAB), and 195 (44.3%) were intubated before any
resuscitation was started (ABC). There was no difference in ISS, mechanism, or
comorbidities. Those intubated prior to receiving transfusion had a lower GCS than
those with transfusion initiation prior to intubation (ABC: 4, CAB:9, p = 0.005).
Although mortality was high in both groups, there was no statistically significant
difference (CAB 47% and ABC 50%). In multivariate analysis, initial SBP and initial
GCS were the only independent predictors of death.
Ferrada, P., Callcut, R.A., Skarupa, D.J. et al. Circulation first
– the time has come to question the sequencing of care in the
ABCs of trauma; an American Association for the Surgery of
Trauma multicenter trial. World J Emerg Surg 13, 8 (2018).

47. AIRWAY
• In patients of shock, the first step is to ensure a clear airway.
• Signs of airway obstruction include:
- See-saw respirations: Obstruction wherein neck muscles and
accessory muscles of respirations are used for respiration.
- Central Cyanosis (Blue lips & Tongue): A late sign of complete
airway obstruction .
- Stridor: Obstruction at laryngeal level or above.
- Wheeze: Obstruction of lower airways
- Gurgling: Liquid or semi-solid material in upper airway
- Snoring: Occlusion of pharynx by tongue or palate.

48. ANATOMIC CONSIDERATIONS IN CHILDREN
• The position of larynx in children and infants is higher and more anterior
than in adults.
• Smaller airways make children more susceptible to oedema, mucous plugs
and foreign body obstruction.
• Correct positioning:

49. NON-INVASIVE PROCEDURES FOR
RELIEF OF OBSTRUCTION
Chin lift - Head tilt Jaw Thrust

50. INVASIVE PROCEDURES FOR
RELIEF OF OBSTRUCTION
OROPHARYNGE
AL
NASOPHARYNGE
AL
Give oxygen initially at a high inspired concentration (100%):
- Use a mask with an oxygen reservoir. Ensure that the oxygen flow is
sufficient (15 litres per minute) to prevent collapse of the reservoir during
inspiration.
- If you have a pulse oximeter, titrate the oxygen delivery aiming for normal
oxygen saturation levels (94–98%).
- In very sick patients this may not be possible and a lower oxygen
saturation (more than 90%) is acceptable for a short period of time.

52. BREATHING
• After the airway is established, if the victim is not breathing
spontaneously, the following general principles should be
considered:
- Rescue Breathing is performed while maintaining airway in
the chin lift/jaw thrust manoeuvre.
- Rescuer should administer 2 breaths, delivering one breath
each over one second.
- The volume that is delivered should make the chest wall rise.
- In patients with breathing inadequacy, rescue breaths should
be provided every 3 to 5 seconds.
- CPR is initiated when there is no pulse or pulse is <60 beats
per minute.

53. METHODS OF RESCUE BREATHING
• Mouth-to-Mouth
• Mouth-to-Barrier-Device
• Mouth-to-Nose
• Mouth-to-Mouth-and-Nose
• Bag Mask Ventilation
Adults: 1 breath every 5-6 seconds (10-12 breaths/min)
Infants & Children: 1 breath every 3-5 seconds (12-20 breaths/min)
Deliver each breath in 1 second
Visible chest rise
Check pulse every 2 minutes

54. • Self-inflating ventilation bag requires an oxygen reservoir system to
reliably deliver oxygen concentrations above 40 percent. This is because
room air is entrained in the system when the bag reinflates.
• With an oxygen flow rate of 15 L/min, oxygen concentrations between 95
and 100% can be delivered using a 2.5 L bag reservoir system.
• The ventilation bag should have a minimum volume of 450 to 500 mL.
Bag-Mask
Ventilation

55. Rescuers Ventilations Compressions
1 2 30
2 2 15
COMPRESSIONS
Increase in intrathoracic pressure
Causes the blood to flow forward
Forces respiratory gases from lungs
Gradual increase in circulatory flow

56. VOLUME RESUSCITATION

57. CRYSTALLOIDS VS COLLOIDS

58. - Colloids are superior to crystalloids in maintain blood volume and
minimizing the shock level. However, because of their expense and less
availability, crystalloids are more commonly used. Hence, normal saline &
Ringer’s Lactate are more commonly used.
- 1L of Normal Saline raises blood volume by 300 mL.
- 1L of Ringer’s Lactate contains lactate, ions of Na, Cl, K, Ca.
- Fluid resuscitation continues up until a normal central venous pressure
has been established.

59. DRUGS USED IN
VARIOUS TYPES OF SHOCK

60. DRUG
GROUP
SHOCK CONTRA-
INDICATIONS
ADULTS CHILDREN
Sedatives Traumatic
Shock
Head Injuries,
Acute Abdomen
Morphine (2.5-10
mg)
Barbiturates,
Largactil(0.55m
g/kg) (head
injury)
Ionotropic
agents
Cardiogenic
& Septic
Shock
Dopamine
insensitivity in
children
Dobutamine
(A: 5-20 mcg/kg/min i.v.,
C: 2-20 mcg/kg/min i.v.)
Dopamine
(3-20 mcg/kg/min i.v.)
Vaso-
dilators
Septic,
Traumatic,
Cardiogenic
Shock
Overdose leads
to low systemic
arterial pressure
Nitroprusside (0.3 mcg/kg/min),
Nitroglycerin (5-10 mcg/min),
Inhaled Nitric Oxide in neonates (20
ppm)
Vaso-
constricto
rs
Neurogenic
Shock
History of
Cardiac
dysfunction
Phenylephrine (50-250
mcg i.v. bolus)
Epinephrine
(0.1 mcg/kg
i.v.)
Beta-
Blockers
Cardiogenic
Shock
Induces slow
heart rate
Propranolol
(A: 120-240 mg, C: 1-5 mcg/kg)
Diuretics Cardiogenic
Shock
Causes
Hypovolemia
Furosemide
(A: 40 mg i.v., C:1-6 mg/kg)

61. ANAPHYLAXIS - CHAIRSIDE
• Most commonly encountered form of shock in dental practice
ETIOLOGY
- Exposure to allergen (latex)
- Foods like peanuts, fish, milk
- Medications like penicillin & its derivatives
- Bee Stings
- Local Anaesthesia (positive aspiration)
DIAGNOSIS
- Face: Itching, Redness, Swelling
- Airway: Coughing, Wheezing, Respiratory distress
- Stomach: Pain, Nausea, Vomiting, Diarrhoea
- Total Body: Rashes, Paleness, Weakness, Loss of consciousness

62. CHAIRSIDE MANAGEMENT
AGE DOSAGE (1:1000)
Infants 0.075 mg
Children 0.15 mg
Adults 0.3 mg

63. CONCLUSION

64. REFERENCES
• Hall, J. (2015). Guyton and Hall textbook of medical physiology. Elsevier.
• Sethuraman, U., & Bhaya, N. (2008). Pediatric shock. Therapy, 5(4), 405–
423.
• Ralston ME. (2019), Basic Airway Management in Children. In J. Wiley
(Ed.), UpToDate, Retrieved Oct 15, 2019.
• Churchill Livingstone. (2015). Scullys Medical Problems in Dentistry
(Seventh Edition).
• Fleeger E. & Kleinman M. (2019), Pediatric Advanced Life Support
(PALS)., In J. Wiley (Ed.), UpToDate, Retrieved Dec 16,2019.
• Das, S. (2008). A concise textbook of surgery. Calcutta: Dr S. Das.
• Fleisher, G. R., Ludwig, S., Bachur, R. G., & Shaw, K. N. (2015). Textbook
of pediatric emergency medicine. Philadelphia: Wolters Kluwer/Lippincott
Williams & Wilkins Health.
• Prasad KD, Hegde C, Alva H, Shetty M. Medical and dental emergencies
and complications in dental practice and its management. J Educ Ethics