Shock.ppt

SEMINAR-4
Presented by
Dr.Akhil C A
First Year PG
Dept.Of .Public Health Dentistry
SCB Dental College And Hospital ,Cuttack
2

CONTENTS
INTRODUCTION
CLASSIFICATION AND ETIOLOGY OF SHOCK
PATHOGENESIS
PATHOPHYSIOLOGY(STAGES OF SHOCK)
CLINICAL FEATURES AND COMPLICATIONS
RESUSCITATION
CLINICAL SIGNIFICANCE
CONCLUSION
REFERENCES
3

INTRODUCTION
• If a systemic complication occurs in dental practice, the dentist is obligated
to make a prompt diagnosis and provide emergency treatment as soon as
possible.
• Therefore, the dentist must be fully aware of medical complications that may
occur in dental practice.
• Emergencies during dental treatment can be classified by etiology into two
major groups: complications associated with an underlying disorder
and those independent of pre-existing disease.
• The main systemic complications include ;(a) shock (b) hyperventilation
syndrome; (c) local anesthetic intoxication; and (d) allergic reaction to
local anesthetics.
4
Niwa, H, Shibutani T, Matsuura H. Systemic Emergencies and their Management in Dentistry: Complications Independent of Underlying Disease. Anesth Prog . 1996;43(2):29–35

• Shock forms one of the important systemic complication that can arise without
an underlying cause or disease.
Definition
• Shock is a systemic state of low tissue perfusion, which is inadequate for normal
cellular respiration. With insufficient delivery of oxygen and glucose, cells switch
from aerobic to anaerobic metabolism. If perfusion is not restored in a timely
fashion, cell death ensues.
-Bailey And Love
• Shock means ‘circulatory failure’. It can be defined as a level of oxygen delivery
that fails to meet the metabolic requirements of the tissues
-Davidson
5
Ralston S, J. SMW, Britton R, Penman ID, Hobson RP. Davidson's principles & practice of medicine. 23rd ed. Edinburgh i 6 pozostałych: Elsevier; 2018.
Williams NS, O'Connell PR, McCaskie AW. Bailey & Love's short practice of surgery. 25th ed. Boca Raton: Edward Arnold Ltd; 2008.
Introduction

Shock is a life-threatening clinical syndrome of cardiovascular collapse
characterised by:
• An acute reduction of effective circulating blood volume (hypotension); and
• An inadequate perfusion of cells and tissues(hypoperfusion).
• If uncompensated, these mechanisms may lead to impaired cellular
metabolism and death.
• Thus, by definition “true (or secondary) shock” is a circulatory imbalance
between oxygen supply and oxygen requirements at the cellular level, and is
also called as circulatory shock.
5
Mohan H, Damjanov I. Textbook of pathology. 6th ed. New Delhi: Jaypee Brothers Medical Publishers; 2010.
Introduction

• The term “initial (or primary) shock” is used for transient and usually a
benign vasovagal attack immediately following trauma, severe pain or
emotional overreaction such as due to fear, sorrow or surprise.
• In routine clinical practice, however, true shock is the form which occurs due
to haemodynamic derangements with hypoperfusion of the cells; this is the
type which is commonly referred to as ‘shock’ if not specified.
6
Introduction

CLASSIFICATION AND ETIOLOGY OF SHOCK
Broadly classified in to;
1. HYPOVOLAEMIC SHOCK
2. CARDIOGENIC SHOCK
3. SEPTIC SHOCK
4. OTHER TYPES
8

1. Hypovolemic shock.
• Hypovolemic shock is a condition of inadequate organ perfusion caused by
loss of intravascular volume, usually acute.
• This form of shock results from inadequate circulatory blood volume by
various etiologic factors that may be either from the loss of red cell mass
and plasma from haemorrhage, or from the loss of plasma volume alone.
Etiology;
i) Acute haemorrhage
ii) Dehydration from vomiting, diarrhoea
iii) Burns
iv) Excessive use of diuretics
v) Acute pancreatitis
9
Classification And Etiology Of Shock

2. Cardiogenic shock.
• Acute circulatory failure with sudden fall in cardiac output from acute
diseases of the heart without actual reduction of blood volume
(normovolaemia) results in cardiogenic shock.
• Etiology;
i) Deficient emptying
e.g.
a) Myocardial infarction
b) Cardiomyopathies
c) Rupture of the heart, ventricle or papillary muscle
c) Cardiac arrhythmias
10

ii) Deficient filling
e.g.
a) Cardiac tamponade from haemopericardium
iii) Obstruction to the outflow
e.g.
a) Pulmonary embolism
b) Ball valve thrombus
c) Tension pneumothorax
d) Dissecting aortic aneurysm
11

3. Septic (Toxaemic) shock.
Severe bacterial infections or septicaemia induce septic shock. It may be the
result of Gramnegative septicaemia (endotoxic shock) which is more common,
or Gram-positive septicaemia (exotoxic shock).
Etiology
i) Gram-negative septicaemia (endotoxic shock)
e.g; Infection with E. coli, Proteus, Klebsiella, Pseudomonas and bacteroides
ii) Gram-positive septicaemia (exotoxic shock) e.g;Infection with streptococci,
pneumococci
13

4. Other types.
i) Traumatic shock.
• Shock resulting from trauma is initially due to hypovolaemia, but even after
haemorrhage has been controlled, these patients continue to suffer loss of plasma
volume into the interstitium of injured tissue and hence is considered separately .
• ii) Neurogenic shock.
• Neurogenic shock results from causes of interruption of sympathetic vasomotor
supply.
iii) Hypoadrenal shock.
• Hypoadrenal shock occurs from unknown adrenal insufficiency in which the patient
fails to respond normally to the stress of trauma, surgery or illness.
14

PATHOGENESIS
In general, all forms of shock involve following 3 derangements:
1. Reduced effective circulating blood volume.
2. Reduced supply of oxygen to the cells and tissues with resultant anoxia.
3. Inflammatory mediators and toxins released from shock induced cellular
injury.
• These derangements initially set in compensatory mechanisms but
eventually a vicious cycle of cell injury and severe cellular dysfunction lead
to breakdown of organ function.
15

1. Reduced effective circulating blood volume.
It may result by either of the following mechanisms:
• By actual loss of blood volume as occurs in hypovolemic shock
• By decreased cardiac output without actual loss of blood (normovolemia) as
occurs in cardiogenic shock and septic shock.
16
pathogenesis

2. Impaired tissue oxygenation.
Following reduction in the effective circulating blood volume from either of the above
two mechanisms and from any of the etiologic agents, there is;
• Decreased venous return to the heart resulting in decreased cardiac output.
• This consequently causes reduced supply of oxygen to the organs and tissues and
hence tissue anoxia, which sets in cellular injury.
16
pathogenesis

3. Release of inflammatory mediators.
• In response to cellular injury, innate immunity gets activated and release
inflammatory mediators
• But eventually these agents themselves become the cause of cell injury.
• Endotoxins in bacterial wall in septic shock stimulate massive release of pro-
inflammatory mediators (cytokines).
• Several pro-inflammatory inflammatory mediators are released from
monocytes-macrophages, other leucocytes and other body cells, the most
important being the tumour necrosis factor- (TNF)-α and interleukin-1 (IL-1)
cytokines .
18
pathogenesis

PATHOGENESIS
19

PATHOGENESIS OF HYPOVOLAEMIC SHOCK.
• Occurs from inadequate circulating blood volume .
• The major effects are due to decreased cardiac output and low intracardiac
pressure.
• The severity of clinical features depends upon degree of blood volume lost,
haemorrhagic shock is divided into 4 types:
• < 1000 ml: Compensated
• 1000-1500 ml: Mild
• 1500-2000 ml: Moderate
• >2000 ml: Severe
20
pathogenesis

• Accordingly, clinical features are increased heart rate (tachycardia), low
blood pressure (hypotension), low urinary output (oliguria to anuria) and
alteration in mental state .
Mild shock
• Initially there is tachycardia, tachypnoea and a mild reduction in urine output
and the patient may exhibit mild anxiety.
• Blood pressure is maintained although there is a decrease in pulse
pressure.
• The peripheries are cool and sweaty with prolonged capillary refill times
(except in septic).
21
pathogenesis

Moderate shock
• As shock progresses, renal compensatory mechanisms fail, renal perfusion
falls and urine output dips .
• Thereis further tachycardia and now the blood pressure starts to fall.
• Patients become drowsy and mildly confused.
Severe shock
• In severe shock there is profound tachycardia and hypotension.
• Urine output falls to zero and patients are unconscious with laboured
respiration
22
pathogenesis

PATHOGENESIS OF CARDIOGENIC SHOCK.
• Cardiogenic shock results from a severe left ventricular dysfunction from
various causes.
• The resultant decreased cardiac output has its effects in the form of
decreased tissue perfusion and movement of fluid from pulmonary vascular
bed into pulmonary interstitial space initially (interstitial pulmonary oedema)
and later into alveolar spaces (alveolar pulmonary oedema).
23
pathogenesis

Pathophysiology-cardiogenic Shock
24
pathogenesis

PATHOGENESIS OF SEPTIC SHOCK.
• Septic shock results most often from Gram-negative bacteria entering the
body from genitourinary tract, alimentary tract, respiratory tract or skin, and
less often from Gram-positive bacteria.
• There is immune system activation and severe systemic inflammatory
response to infection as;
i) Activation of macrophage-monocytes.
• Lysis of Gramnegative bacteria releases endotoxin, lipopolysaccharide, into
circulation where it binds to lipopolysaccharide-binding protein (LBP).
25
pathogenesis

• The complex of LPS-LBP binds to CD14 molecule on the surface of the
monocyte/macrophages which are stimulated to elaborate cytokines, the
most important ones being TNF-α and IL-1.
The effects of these cytokines are;
• By altering endothelial cell adhesiveness: This results in recruitment of more
neutrophils which liberate free radicals that cause vascular injury.
• Promoting nitric oxide synthase: This stimulates increased synthesis of nitric
oxide which is responsible for vasodilatation and hypotension.
26
pathogenesis

ii) Activation of other inflammatory responses.
a) Activation of complement pathway: End-products C5a and C3a induce
microemboli and endothelial damage.
b) Activation of mast cells: Histamine is released which increases capillary
permeability.
c) Activation of coagulation system: Enhances development of thrombi.
d) Activation of kinin system: Released bradykinin cause vasodilatation and
increased capillary permeability.
27
pathogenesis

• The net result of above mechanisms is vasodilatation and increased
vascular permeability in septic shock.
• Profound peripheral vasodilatation and pooling of blood causes
hyperdynamic circulation in septic shock, in contrast to hypovolaemic and
cardiogenic shock.
• Increased vascular permeability causes development of inflammatory
oedema.
• Disseminated intravascular coagulation (DIC) is prone to develop in septic
shock due to endothelial cell injury by toxins.
• Reduced blood flow produces hypotension, inadequate perfusion of cells
and tissues, finally leading to organ dysfunction.
28
pathogenesis

PATHOGENESIS OF SEPTIC SHOCK 29
pathogenesis

PATHOPHYSIOLOGY (Stages of Shock)
• Although deterioration of the circulation in shock is a progressive and
continuous phenomenon and compensatory mechanisms become
progressively less effective, historically shock has been divided arbitrarily
into 3 stages
1. Compensated (non-progressive, initial, reversible) shock.
2. Progressive decompensated shock.
3. Irreversible decompensated shock.
30

1. COMPENSATED (NON-PROGRESSIVE, INITIAL,REVERSIBLE)
SHOCK.
• In the early stage of shock, an attempt is made to maintain adequate
cerebral and coronary blood supply by redistribution of blood so that the vital
organs (brain and heart) are adequately perfused and oxygenated.
• This is achieved by activation of various neurohormonal mechanisms
causing widespread vasoconstriction and by fluid conservation by the
kidney.
• If the condition that caused the shock is adequately treated, the
compensatory mechanism may be able to bring about recovery and
reestablish the normal circulation.
Pathophysiology
31

i) Widespread vasoconstriction.
ii) Fluid conservation by the kidney.
iii) Stimulation of adrenal medulla.
I. Widespread vasoconstriction.
• In response to reduced blood flow (hypotension) and tissue anoxia, the
neural and humoral factors (e.g. baroreceptors, chemoreceptors,
catecholamines, renin, and angiotensin-II) are activated.
• All these bring about vasoconstriction, particularly in the vessels of the skin
and abdominal viscera. Widespread vasoconstriction is a protective
mechanism as it causes increased peripheral resistance, increased heart
rate (tachycardia) and increased blood pressure.
MECHANISMS OF COMPENSATION
32
Pathophysiology

• However, in septic shock, there is initial vasodilatation followed by
vasoconstriction.
• Besides, in severe septic shock there is elevated level of thromboxane A2
which is a potent vasoconstrictor and may augment the cardiac output along
with other sympathetic mechanisms.
• Clinically cutaneous vasoconstriction is responsible for cool and pale skin in
initial stage of shock
33
Pathophysiology

ii. Fluid conservation by the kidney.
In order to compensate the actual loss of blood volume in hypovolaemic
shock,the following factors may assist in restoring the blood volume and
improve venous return to the heart:
• Release of aldosterone from hypoxic kidney by activation of renin-
angiotensin-aldosterone mechanism.
• Release of ADH due to decreased effective circulating blood volume.
• Reduced glomerular filtration rate (GFR) due to arteriolar constriction.
34
Pathophysiology

iii) Stimulation of adrenal medulla.
• In response to low cardiac output, adrenal medulla is stimulated to release
excess of catecholamines (epinephrine and non-epinephrine) which
increase heart rate and try to increase cardiac output.
36
Pathophysiology

2.PROGRESSIVE DECOMPENSATED SHOCK.
• This is a stage when the patient suffers from some other stress or risk
factors besides persistence of the shock so that there is progressive
deterioration.
• The effects are due to tissue hypoperfusion are as under:
i) Pulmonary hypoperfusion.
Decompensated shock worsens pulmonary perfusion and increases vascular
permeability resulting in tachypnoea and acutes respiratory distress syndrome
(ARDS).
37
Pathophysiology

• ii) Tissue ischaemia.
• Impaired tissue perfusion causes switch from aerobic to anaerobic
glycolysis resulting in metabolic lactic acidosis.
• Lactic acidosis lowers the tissue pH which in turn makes the vasomotor
response ineffective.
• This results in vasodilatation and peripheral pooling of blood.
• Clinically at this stage the patient develops confusion and worsening of renal
function.
38
Pathophysiology

3.IRREVERSIBLE DECOMPENSATED SHOCK.
• When the shock is so severe that in spite of compensatory mechanisms and
despite therapy and control of etiologic agent which caused the shock, no
recovery takes place, it is called decompensated or irreversible shock.
• Its effects due to widespread cell injury include the following:
i) Progressive vasodilatation.
• During later stages of shock, anoxia damages the capillary and venular wall
and arteioles become unresponsive to vasoconstrictors listed above and
begin to dilate.
• Vasodilatation results in peripheral pooling of blood which further deteriorate
the effective circulating blood volume.
39
Pathophysiology

ii) Increased vascular permeability.
• Anoxic damage to tissues releases inflammatory mediators which cause
increased vascular permeability.
• This results in escape of fluid from circulation into the interstitial tissues thus
deteriorating effective circulating blood volume.
iii) Myocardial depressant factor (MDF).
• Progressive fall in the blood pressure and persistently reduced blood flow to
myocardium causes coronary insufficiency and myocardial ischaemia due to
release of myocardial depressant factor (MDF).
• This results in further depression of cardiac function, reduced cardiac output
and decreased blood flow.
40
Pathophysiology

iv) Worsening pulmonary hypoperfusion.
• Further pulmonary hypoperfusion causes respiratory distress due to
pulmonary oedema, tachypnoea and acute respiratory distress syndrome
(ARDS).
v) Anoxic damage to heart, kidney, brain.
• Progressive tissue anoxia causes severe metabolic acidosis due to
anaerobic glycolysis.
• There is release of inflammatory cytokines and other inflammatory
mediators and generation of free radicals.
• Since highly specialized cells of myocardium, proximal tubular cells of the
kidney, and neurons of the CNS are dependent solely on aerobic respiration
for ATP generation, there is ischaemic cell death in these tissues.
41
Pathophysiology

vi) Hypercoagulability of blood.
• Tissue damage in shock activates coagulation cascade with release of clot
promoting factor, thromboplastin and release of platelet aggregator, ADP,
which contributes to slowing of blood-stream and vascular thrombosis.
• In this way, hypercoagulability of blood with consequent microthrombi impair
the blood flow and cause further tissue necrosis.
• Clinically, at this stage the patient has features of coma, worsened heart
function and progressive renal failure due to acute tubular necrosis.
42
Pathophysiology

MECHANISMS AND EFFECTS OF THREE STAGES OF
SHOCK
43
Pathophysiology

CLINICAL FEATURES AND COMPLICATIONS
• The classical features of decompensated shock are characterised by
depression of 4 vital processes:
1. Very low blood pressure
2. Subnormal temperature
3. Feeble and irregular pulse
4. Shallow and sighing respiration
• In addition, the patients in shock have pale face, sunken eyes, weakness,
cold and clammy skin.
44

Clinical Features
45
Clinical Features And
Complications

• Life-threatening complications in shock are due to hypoxic cell injury
resulting in immuno-inflammatory responses and activation of various
cascades (clotting, complement, kinin). These include the following:
1. Acute respiratory distress syndrome (ARDS)
2. Disseminated intravascular coagulation (DIC)
3. Acute renal failure (ARF)
4. Multiple organ dysfunction syndrome (MODS)
• With progression of the condition, the patient may develop stupor, coma and
death.
46
Complications

Pitfalls
• The classic cardiovascular responses described are not seen in every
patient.
Capillary refill
• Most patients in hypovolaemic shock will have cool, pale peripheries with
prolonged capillary refill times; however, the actual capillary refill time varies
so much in adults that it is not a specific marker of whether a patient is
shocked, and patients with short capillary refill times may be in the early
stages of shock.
• In distributive (septic) shock the peripheries will be warm and capillary refill
will be brisk despite profound shock.
47
Complications

Tachycardia
• Tachycardia may not always accompany shock.
• Patients who are on β-blockers or who have implanted pacemaker are
unable to mount a tachycardia.
• A pulse rate of 80 in a fit young adult who normally has a pulse rate of 50 is
very abnormal.
• Furthermore, in some young patients with penetrating trauma, when there is
haemorrhage but little tissue damage, there may be a paradoxical
bradycardia rather than tachycardia accompanying the shocked state.
48
Complications

Blood pressure
• It is important to recognise that hypotension is one of the last signs of shock.
• Children and fit young adults are able to maintain blood pressure until the final
stages of shock by dramatic increases in stroke volume and peripheral
vasoconstriction.
• These patients can be in profound shock with a normal blood pressure.
• Elderly patients who are normally hypertensive may present with a ‘normal’
blood pressure for the general population but be hypovolaemic and hypotensive
relative to their usual blood pressure.
49
Complications

Consequences
Unresuscitatable shock
• Patients who are in profound shock for a prolonged period of time become
‘unresuscitatable’. Cell death follows from cellular ischaemia, and the ability
of the body to compensate is lost.
• There is myocardial depression and loss of responsiveness to fluid or
inotropic therapy. Peripherally there is loss of the ability to maintain systemic
vascular resistance and further hypotension ensues.
• The peripheries no longer respond appropriately to vasopressor agents.
50
Complications

Multiple organ failure
• Multiple organ failure is defined as two or more failed organ systems There
is no specific treatment for multiple organ failure.
• Management is by supporting organ systems with ventilation, cardiovascular
support and haemofiltration/dialysis until there is recovery of organ function.
• Multiple organ failure currently carries a mortality rate of 60%. Thus,
prevention is vital by early aggressive identification and reversal of shock.
51
Complications

• The major organs affected are the brain, heart, lungs and kidneys.
Morphologic changes are also noted in the adrenals, gastrointestinal tract,
liver and other organs.
1. HYPOXIC ENCEPHALOPATHY.
• Cerebral ischaemia in compensated shock may produce altered state of
consciousness.
• However, if the blood pressure falls below 50 mmHg as occurs in systemic
hypotension in prolonged shock and cardiac arrest, brain suffers from
serious ischaemic damage with loss of cortical functions, coma, and a
vegetative state.
52
Complications

2. HEART IN SHOCK.
• Heart is more vulnerable to the effects of hypoxia than any other organ.
• Heart is affected in cardiogenic as well as in other forms of shock. There are
2 types of morphologic changes in heart in all types of shock:
i) Haemorrhages and necrosis. There may be small or large ischaemic areas
or infarcts, particularly located in the subepicardial and subendocardial region.
ii)Zonal lesions. These are opaque transverse contraction bands in the
myocytes near the intercalated disc.
53
Complications

3. SHOCK LUNG.
Lungs due to dual blood supply are generally not affected by hypovolaemic
shock but in septic shock the morphologic changes in lungs are quite
prominent termed ‘shock lung’.
• Grossly, the lungs are heavy and wet.
• Microscopically, changes of acute respiratory distress syndrome (ARDS) are
seen.
• Briefly, the changes include congestion, interstitial and alveolar oedema,
interstitial lymphocytic infiltrate, alveolar hyaline membranes, thickening and
fibrosis of alveolar septa, and fibrin and platelet thrombi in the pulmonary
microvasculature.
54
Complications

• 4. SHOCK KIDNEY.
• One of the important complications of shock is irreversible renal injury, first
noted in persons who sustained crush injuries in building collapses in air
raids in World War II.
• The renal ischaemia following systemic hypotension is considered
responsible for renal changes in shock. The end-result is generally anuria
and death.
• Microscopically, the tubular lesions are seen at all levels of nephron and are
referred to as acute tubular necrosis (ATN) which can occur following
other causes besides shock .
55
Complications

5. ADRENALS IN SHOCK.
• The adrenals show stress response in shock.
• This includes release of aldosterone in response to hypoxic kidney, release
of glucocorticoids from adrenal cortex and catecholamines like adrenaline
from adrenal medulla.
• In severe shock, acute adrenal haemorrhagic necrosis may occur.
56
Complications

6.HAEMORRHAGIC GASTROENTEROPATHY.
• The hypoperfusion of the alimentary tract in conditions such as shock and
cardiac failure may result in mucosal and mural infarction called
haemorrhagic gastroenteropathy.
• In shock due to burns, acute stress ulcers of the stomach or duodenum may
occur and are known as Curling’s ulcers.
• Secondary infection may supervene and condition may progress into
pseudomembranous enterocolitis.
57
Complications

7. LIVER IN SHOCK.
• Grossly, faint nutmeg appearance is seen.
• Microscopically, depending upon the time lapse between injury and cell
death, ischaemic shrinkage, focal necrosis, or fatty change may be seen.
• Liver function may be impaired.
8. OTHER ORGANS.
Other organs such as lymph nodes, spleen and pancreas may also show foci
of necrosis in shock.
58
Complications

RESUSCITATION
• Immediate resuscitation manoeuvres for patients presenting in shock are to
ensure a patent airway and adequate oxygenation and ventilation.
• Once ‘airway’ and ‘breathing’ are assessed and controlled, attention is
directed to cardiovascular resuscitation.
Conduct of resuscitation
• Resuscitation should not be delayed in order to definitively diagnose the
source of the shocked state.
59

• Rapid clinical examination will provide adequate clues to make an
appropriate first determination, even if a source of bleeding or sepsis is not
immediately identifiable.
• If there is initial doubt about the cause of shock it is safer to assume the
cause is hypovolaemia and begin with fluid resuscitation, followed by an
assessment of the response.
• In patients who are actively bleeding (major trauma, aortic aneurysm
rupture, gastrointestinal haemorrhage) it is counterproductive to institute
high-volume fluid therapy without controlling the site of haemorrhage.
60
Resuscitation

• Increasing blood pressure merely increases bleeding from the site, and fluid
therapy cools the patient and dilutes available coagulation factors.
• Thus, operative haemorrhage control should not be delayed and
resuscitation should proceed in parallel with surgery.
61
Resuscitation

Fluid therapy
• In all cases of shock, regardless of classification, hypovolaemia and
inadequate preload must be addressed before other therapy is instituted.
• Administration of inotropic or chronotropic agents to an empty heart will
rapidly and permanently deplete the myocardium of oxygen stores and
dramatically reduce diastolic filling and therefore coronary perfusion.
62
Resuscitation

• Patients will enter the unresuscitatable stage of shock as the myocardium
becomes progressively more ischaemic and unresponsive to resuscitative
attempts.
• First-line therapy, therefore, is intravenous access and administration of
intravenous fluids.
63
Resuscitation

TYPE OF FLUIDS
• There is no ideal resuscitation fluid for the management of shock
it is more important to understand how and when to administer
them.
• In most studies of shock resuscitation there is no overt difference in
response or outcome between crystalloid solutions (normal saline,
Hartmann’s solution, Ringer’s lactate) and colloids (albumin or commercially
available products).
64
Resuscitation

• On balance there is little evidence to support the administration of colloids,
which are more expensive and have worse side-effect profiles.
• Most importantly, the oxygen-carrying capacity of crystalloids and colloids is
zero.
• If blood is being lost, the ideal replacement fluid is blood, although crystalloid
therapy may be required while awaiting blood products.
• Hypotonic solutions (e.g. dextrose) are poor volume expanders and should
not be used in the treatment of shock unless the deficit is free water loss
(e.g. diabetes insipidus) or patients are sodium overloaded (e.g. cirrhosis).
65
Resuscitation

Dynamic fluid response
• The shock status can be determined dynamically by the cardiovascular
response to the rapid administration of a fluid bolus.
• In total, 250–500 ml of fluid is rapidly given (over 5–10 min) and the
cardiovascular responses in terms of heart rate, blood pressure and central
venous pressure (CVP) are observed.
• Patients can be divided into ‘responders’, ‘transient responders’ and
‘nonresponders’.
66
Resuscitation

• Responders show an improvement in their cardiovascular status, which is
sustained. These patients are not actively losing fluid but require filling to a
normal volume status.
• Transient responders show an improvement but then revert to their
previous state over the next 10–20 min. These patients either have
moderate on-going fluid losses (either overt haemorrhage or further fluid
shifts reducing intravascular volume).
• Non-responders are severely volume depleted and are likely to have major
on-going loss of intravascular volume, usually through persistent
uncontrolled haemorrhage.
67
Resuscitation

Vasopressor and inotropic support
• Vasopressor or inotropic therapy is not indicated as first-line therapy in
hypovolaemia.
• Administration of these agents in the absence of an adequate preload
rapidly leads to decreased coronary perfusion and depletion of myocardial
oxygen reserves.
• Vasopressor agents (phenylephrine, noradrenaline) are indicated in
distributive shock states (sepsis, neurogenic shock), in which there is
peripheral vasodilatation and a low systemic vascular resistance, leading to
hypotension despite a high cardiac output.
68
Resuscitation

• In cardiogenic shock or when myocardial depression complicates a shock
state (e.g. severe septic shock with low cardiac output), inotropic therapy
may be required to increase cardiac output and, therefore, oxygen delivery.
• The inodilator dobutamine is the agent of choice.
69
Resuscitation

Monitoring
• The minimum standard for monitoring of the patient in shock is continuous
heart rate and oxygen saturation monitoring, frequent non-invasive blood
pressure monitoring and hourly urine output measurements.
• Most patients will need more aggressive invasive monitoring including CVP
and invasive blood pressure monitoring
70
Resuscitation

71
Resuscitation

Cardiovascular
• As a minimum, cardiovascular monitoring should include continuous heart
rate [electrocardiogram (ECG)], oxygen saturation and pulse waveform and
non-invasive blood pressure.
• Patients whose state of shock is not rapidly corrected with a small amount of
fluid should have CVP monitoring and continuous blood pressure monitoring
through an arterial line.
72
Resuscitation

Central venous pressure
• There is no ‘normal’ CVP for a shocked patient, and reliance cannot be
placed on an individual pressure measurement to assess volume status.
Some patients may require a CVP of 5 cmH2O, whereas others may require
a CVP of 15 cmH2O or higher.
• Further, ventricular compliance can change from minute to minute in the
shocked state, and CVP is a poor reflection of end-diastolic volume
(preload).
73
Resuscitation

• CVP measurements should be assessed dynamically as the response to a
fluid challenge.
• A fluid bolus (250–500 ml) is infused rapidly over 5–10 min.
• The normal CVP response is a rise of 2–5 cmH2O, which gradually drifts
back to the original level over 10–20 min.
• Patients with no change in their CVP are empty and require further fluid
resuscitation.
• Patients with a large, sustained rise in CVP have high preload and an
element of cardiac insufficiency or volume overload.
74
Resuscitation

Cardiac output
• Measurement of cardiac output, systemic vascular resistance and preload
can help distinguish the types of shock that are present (hypovolaemia,
distributive, cardiogenic), especially when they coexist.
• Invasive cardiac monitoring using pulmonary artery catheters is becoming
less frequent as new non-invasive monitoring techniques such as Doppler
ultrasound, pulse waveform analysis and indicator dilution methods provide
similar information without many of the drawbacks of more invasive
techniques.
75
Resuscitation

Systemic and organ perfusion
• Ultimately, the goal of treatment is to restore cellular and organ perfusion.
• The best measures of organ perfusion and the best monitor of the adequacy
of shock therapy remain the urine output; however, this is an hourly measure
and does not give a minute-to-minute view of the shocked state.
• The level of consciousness is an important marker of cerebral perfusion, but
brain perfusion is maintained until the very late stages of shock and, hence,
is a poor marker of adequacy of resuscitation.
76
Resuscitation

• Currently, the only clinical indicators of perfusion of the gastrointestinal tract
and muscular beds are the global measures of lactic acidosis (lactate and
base deficit) and the mixed venous oxygen saturation.
Base deficit and lactate
• Lactic acid is generated by cells undergoing anaerobic respiration.
• The degree of lactic acidosis, as measured by the serum lactate level and/or
the base deficit, is a sensitive tool for both the diagnosis of shock and the
monitoring of the response to therapy.
• Patients with a base deficit of over 6 mmol/L have much higher morbidity
and mortality rates than those with no metabolic acidosis.
77
Resuscitation

• Further, the duration of time in shock with an increased base deficit is
important, even if all other vital signs have returned to normal (occult
hypoperfusion).
• These parameters are measured from arterial blood gas analyses and,
therefore, the frequency of measurements is limited and they do not provide
minute-to-minute data on systemic perfusion or the response to therapy.
• Nevertheless, the base deficit and/or lactate should be measured routinely in
these patients until they have returned to normal levels.
78
Resuscitation

Mixed venous oxygen saturation
• The percentage saturation of oxygen returning to the heart from the body is a
measure of the oxygen delivery and extraction by the tissues.
• Normal mixed venous oxygen saturation levels are 50–70%.
• Levels below 50% indicate inadequate oxygen delivery and increased oxygen
extraction by the cells.
• This is consistent with hypovolaemic or cardiogenic shock.
• High mixed venous saturation levels (> 70%) are seen in sepsis as there is
disordered utilisation of oxygen at the cellular level.
79

DENTAL IMPLICATIONS
Mostly encountered forms of shock in dental setting are;
• Syncope/neurogenic shock
• Anaphylactic shock
• Hypovolemic shock
• Septic shock
80

SYNCOPE
• Neurogenic shock or syncope, also called vasovagal syncope and acute
cerebral anemia, is the most common systemic complication in dentistry.
• A sudden,transient loss of consciousness without prodromal symptoms that
is followed within seconds to minutes (<30 minutes) by resumption of
consciousness.
• Some investigators may call it syncope in mild cases and neurogenic shock
in severe instances, as the patients manifest signs and symptoms of varying
intensity.
81
Malamed SF. Medical emergencies in the dental office. 7th ed. St. Louis: Mosby; 2015.

MECHANISM
Dilation of the peripheral arterioles
Failure of normal peripheral vasoconstrictor activity
(orthostatic hypotension)
A significant drop in cardiac output (from heart disease,
dysrhythmias, or decreased blood volume)
Constriction of cerebral vessels as carbon dioxide is lost through
hyperventilation
Occlusion or narrowing of the internal carotid or other arteries to the
brain
Life-threatening ventricular dysrhythmias
82

MANAGEMENT
Step 1: Assessment of consciousness.
Step 2: Termination of dental procedure.
Step 3: Activate office emergency team
Step 4: Place unconscious victim in supine position with feet elevated
Step 5: Assess circulation.
Step 6: Assess and open airway.
Step 7a: Assess airway patency and breathing.
Step 7b: Rescue breathing (if necessary).
Step 8: Definitive management.
83

in the trendelenburg position, the victim should be tilted back even further in the dental chair so that
the head is below the level of the heart and turned to one side.
84

ANAPHYLACTIC SHOCK
• Anaphylactic shock is characterized by massive histamine-mediated
vasodilation and maldistribution with a shift of fluid from the intravascular to the
extravascular space.
• It is a type I hypersensitivity reaction,usually mediated by IgE-antibodies. The
central role is played by mast cells and the histamine they release.
Clinical presentation
• The clinical presentation varies greatly from one individual to another according
to the dose and site of entry of the antigen and the degree of sensitization.
85

• As an early symptom,the patient complains of chest discomfort and itching in
the face and chest.
• Flushing and urticaria develop as a sign of cutaneous system irritation.
Smooth muscle contraction in the gastrointestinal tract provokes
stomachache, vomiting, diarrhea, and fecal or urinary incontinence.
• Retrosternal oppression and chest pain could be the cardiac manifestation.
Wheezing and dyspnea become audible due to bronchospasm.
Furthermore, acute airway obstruction occurs in association with laryngeal
edema.
• Palpitation, tachycardia, arrhythmia, hypotension, loss of consciousness,
and cardiac arrest would take place successively.
86

Treatment
• Anaphylactic shock can be fatal within several minutes of onset. Therefore, the
prognosis depends greatly upon initial treatment in the first 5 min.
• Epinephrine is the drug of first choice in anaphylactic shock. At first, 0.3 to 0.5 mg of
epinephrine is given intramuscularly.
87

88

Anaphylactic Shock-in Dental Setting 89

SEPTIC Shock-in Dental Setting 90

Hypovolemic Shock-in Dental Setting
91

CLINICAL SIGNIFICANCE
• Sahadev et al. (1994) in an autopsy study of 177 RTI deaths noticed that
neurological injury and haemorrhagic shock were responsible for 60% and
25% of deaths, respectively.
• It was concluded that 23% of death were preventable, 46% possibly
preventable and 30% not preventable by any intervention.
• The preventable deaths forms the responsibility of the clinician in the setting.
• Since shock is one of the most important systemic complication that can
arise in the dental setting,the dentist should be able to diagnose and
manage this emergency,promptly.
92

CONCLUSION
• Shock can be due to multiple causes & affect the body at cellular, visceral &
systemic levels.
• Irrespective of the cause, the fundamental primary management of shock
remains recognition & prompt fluid replacement.
• The search for the underlying cause of the shock is only initiated after
stabilization
• In short management of patients with shock calls for a collaborative,
interprofessional approach.
• Clinicians must react promptly to the emergency.
93

REFERENCES
1. Ralston S, Britton R, Penman ID, Hobson RP. Davidson's principles & practice of
medicine. 23rd ed. Edinburgh : Elsevier; 2018.
2. Williams NS, O'Connell PR, McCaskie AW. Bailey & Love's short practice of
surgery. 25th ed. Boca Raton: Edward Arnold Ltd; 2008.
3. Mohan H, Damjanov I. Textbook of pathology. 6th ed. New Delhi: Jaypee Brothers
Medical Publishers; 2010.
4. Santoskar R S, Nirmala N R, Bhandarkar S D.Pharmacology and
pharmacotherapeutics. 24th ed.Bombay: Popular Prakashan; 2015.
5. Malamed SF. Medical emergencies in the dental office. 7th ed. St. Louis: Mosby;
2015.
94

6. Kim H, Lee J, Seo K, Kwon S, Row H. Anaphylactic reaction after local lidocaine
infiltration for retraction of retained teeth. Journal of Dental Anesthesia and Pain
Medicine. 2019;19(3):175.
7. Niwa, H, Shibutani T, Matsuura H. Systemic Emergencies and their Management
in Dentistry: Complications Independent of Underlying Disease. Anesth Prog .
1996;43(2):29–35.
8. Elad S, Chackartchi T, Shapira L, Findler M. A critically severe gingival bleeding
following non-surgical periodontal treatment in patients medicated with anti-
platelet. Journal of Clinical Periodontology. 2008;35(4):342–5.
9. Mannan S, Tordik PA, Martinho FC, Chivian N, Hirschberg CS. Dental Abscess to
Septic Shock: A Case Report and Literature Review. Journal of Endodontics.
2021;20(3) :29–35.
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