Shock is a state of acute circulatory failure leading to decreased organ perfusion, with inadequate delivery of oxygenated blood to tissues and resultant end-organ dysfunction. The mechanisms that can result in shock are divided into 4 categories: (1) hypovolemic, (2) distributive, (3) cardiogenic, and (4) obstructive. While much is known regarding treatment of patients in shock, several controversies continue in the literature. Assessment begins with identifying the need for critical interventions such as intubation, mechanical ventilation, or obtaining vascular access. Prompt workup should be initiated with laboratory testing (especially of serum lactate levels) and imaging, as indicated. Determining the intravascular volume status of patients in shock is critical and aids in categorizing and informing treatment decisions. This issue reviews the 4 primary categories of shock as well as special categories, including shock in pregnancy, traumatic shock, septic shock, and cardiogenic shock in myocardial infarction. Adherence to evidence-based care of the specific causes of shock can optimize a patient's chances of surviving this life-threatening condition.

1. MANAGEMENT OF
SHOCK
Mr. MAHESH. S (M.Sc. Nursing )
Nurse Educator
MGMCRI

2. DEFINITION
• Shock is a physiologic state characterized by systemic
reduction in tissue hypo-perfusion, resulting in
decreased tissue oxygen delivery.
• Shock is initially reversible, but must be recognized
and treated immediately to prevent progression to
irreversible organ dysfunction.

3. CLASSIFICATION OF SHOCK:
Physiological
Hypoxic
Anaemic
Stagnant
Histotoxic
H
A
S
H

4. CLASSIFICATION OF SHOCK:
Clinical
Cardiogenic
Hypovolemic
Obstructive
Distributive
Neurogenic
Septic
Anaphylactic

5. 6

6. 5

7. ETIOLOGICAL FACTORS
Cardiogen
ic
Sudden
"valve
failure"
Drug
overdose
Rate
problem:
too fast or
too slow
AF
Severe
acidosis
Ischaemia

8. ETIOLOGICAL FACTORS
Distributi
ve
Thyroid
insufficiency
(myxoedema)
Adrenal
insufficiency
Angioedema
Drug
overdose (of
vasodilators)
Toxic shock
syndrome
CO2 excess

9. ETIOLOGICAL FACTORS :
INTRA
CARDIAC
Pulmonary
embolism
Valve
obstruction
(thrombosis,
myxoma)
LVOT
obstruction
RVOT
obstruction
EXTRA
CARDIAC
Cardiac
tamponade
Tension
pneumothorax
Dynamic
hyperinflation
Excessive
positive
pressure
ventilation
Restrictive
pericarditis
Chest
compression
(traumatic
asphyxia)
O
B
S
T
R
U
C
T
I
V
E

10. ETIOLOGICAL FACTORS :
• Vomiting
• Diarrhoea
• Polyuria
• Burns
• Ascites
LOSS OF FLUID
H
Y
P
O
V
O
L
E
M
I
C
• Traumatic or surgical
• Uterine
(postpartum)
• Fractures
• Pulmonary/
intrathoracic
• Retroperitoneal or
abdominal
LOSS OF BLOOD

11. PATHOPHYSIOLOGY
INADEQUATE TISSUE
PERFUSION
CELL HYPOXIA
ENERGY DEFICIT
LACTIC ACID ACCUMULATION
& FALL IN PH
METABOLIC ACIDOSIS
CELL MEMBRANE DYSFUNCTION
& FAILURE OF SODIUM PUMP
INTRACELLULAR LYSOSOMES
RELEASE DIGESTIVE ENZYMES
TOXIC SUBSTANCES ENTER
CIRCULATION
CAPILLARY ENDOTHELIUM
DAMAGED
DESTRUCTION, DYSFUNCTION,
CELL DEATH
ANAEROBIC
METABOLISM
EFFLUX OF POTTASSIUM
INFLUS OF Na, WATER
vasoconstriction
Failure of pre capillary
sphincters
Peripheral pooling of blood

12. PATHOPHYSIOLOGY
• When the oxygen level is
low, carbohydrate breaks
down for energy and makes
lactic acid.
• Lactic acid levels get higher
when strenuous exercise or
other conditions-such as
heart failure, a severe
infection (sepsis), or shock,
lower the flow of blood and
oxygen throughout the body.

13. STAGES OF SHOCK Stage 1: Initial Stage
• shock is reversible,
• Doesn't indicate any symptoms of shock at this
stage.
• Cells begin to change due to hypo perfusion and
oxygenation.
• Without this nutritive blood and an adequate
oxygen supply, the cells switch to anaerobic
metabolism, producing pyruvic and lactic acid.

14. STAGES OF SHOCK Stage 2: Compensatory Stage
• Body tries to reverse the results of the initial stage
• Physiological, neural, hormonal, and biochemical
reactions are employed to correct the imbalances.
Hyperventilation is one such mechanism. .
• Increased rate of breathing which, in turn, may
help to get more oxygen flowing to the cells and
neutralize
.

15. STAGES OF SHOCK Stage 2: Compensatory Stage
• Hypotension, or low blood pressure, due to the
reduced volume of blood flow triggers this
response.
• Catecholamine's are hormones released by the
adrenal glands. These hormones increase heart rate
and attempt to increase blood pressure.

16. STAGES OF SHOCK Stage 2: Compensatory Stage
• During this response, a hormone
called vasopressin is released into
the bloodstream. Vasopressin
helps to retain fluid and triggers
vasoconstriction.

17. STAGES OF SHOCK Stage 3: Progressive Stage
• Initial cause is not corrected
• Damages become more severe and can be
irreversible.
• Cellular function continues to deteriorate, anaerobic
metabolism leads to increased metabolic acidosis
• Compensatory mechanisms can no longer maintain
the balance required to protect the organs.

18. STAGES OF SHOCK Stage 4: Refractory Stage
• Irreversible IF cause of shock cannot be fixed
• At this stage, the organs completely fail and lead to
death.
• Identify the cause immediately and resolve it soon

19. STAGES OF SHOCK Stage 4: Refractory Stage
• Irreversible IF cause of shock cannot be fixed
• At this stage, the organs completely fail and lead to
death.
• Identify the cause immediately and resolve it soon

20. SIGNS AND SYMPTOMS
• Rapid, shallow breathing
• Cold, clammy skin
• Rapid, weak pulse
• Dizziness or fainting
• Weakness
• High blood pressure or normal
Initial symptoms

21. SIGNS AND SYMPTOMS
• Persisting tachycardia or bradycardia
• Hypotension- LATE sign!!
• Poor capillary refill
• Altered mental status
• Irregular breathing pattern
• Poor muscle tone
LATER SIGNS

23. DIAGNOSTIC EVALUATION
Empiric Criteria for Diagnosis of Shock
4 out of 6 criteria have to be met
• Decreased LOC or looks ill
• HR > 100
• RR > 22 or PC02 < 32
• Base Deficit < -5 or lactate > 4
• Urine output < 0.5 ml/kg/hr
• Hypotension > 20 min duration

24. ASSESMENT OF SHOCK
Non invasive:
• Perfusion status -mental
status, urine output and
peripheral warmth and
colour
• (SVR = MAP - CVP/CO)
Invasive:
• IABP
• serum lactate levels,
electrolytes and blood gas
estimation including pH
level.
• Thermodilution for CO

25. Thermodilution:
A method of cardiac output
determination. A bolus of solution
of known volume and
temperature is injected into the
right atrium, and the resultant
change in blood temperature is
detected by a thermistor
previously placed in the
pulmonary artery with a catheter.

26. MANAGEMENT OF SHOCK:
Goal:
• Prevention of tissue
hypoxia
• fluid resuscitation with
either crystalloids or
colloids to achieve specific
haemodynamic
HYPOVOLAEMIC SHOCK
• To achieve hemodynamically
stable
CVP of 8–12 mmHg,
MAP >70 mmHg,
urine output >0.5 mL/kg/h

27. MANAGEMENT OF SHOCK: HYPOVOLAEMIC SHOCK
The scientific rationale
for using colloids over
crystalloids is to
preserve plasma oncotic
pressure so as to retain
intravascular fluid and
minimise oedema.

28. MANAGEMENT OF SHOCK:
CARDIOGENIC SHOCK
Inotropic therapy:
Intravenous positive
inotropes promote
myocardial
contractility to
improve cardiac
output and blood
pressure.
IV diuretics
(frusemide) given
usually as intermittent
boluses or if necessary
as a continuous
infusion

29. MANAGEMENT OF SHOCK:
CARDIOGENIC SHOCK
INTRA-AORTIC BALLOON PUMP (IABP)
THERAPY.
The intra-aortic balloon pump is a
mechanical device that increases
myocardial oxygen perfusion while at the
same time increasing cardiac output.
Increasing cardiac output increases
coronary blood flow and therefore myocardial
oxygen delivery.

30. MANAGEMENT OF SHOCK:
CARDIOGENIC SHOCK
video

31. MANAGEMENT OF SHOCK: CARDIOGENIC SHOCK
Respiratory support
CPAP at conventional
levels of 5–15 cmH2O
is well established as a
support for the
spontaneously
breathing patient with
pulmonary oedema.
CPAP Improves hypoxaemia,
lessens WOB, reduces left
ventricular afterload and provides
additional benefit by impeding
venous return, an effect that may
lessen pulmonary congestion.

32. MANAGEMENT OF SHOCK:
SEPTIC SHOCK
Inotropes and vasopressors:
Dobutamine (2.5–10 mcg/kg)
A goal of maintaining MAP greater
than 65 mmHg is common, with
inotropes and vasopressors
commenced when fluid
resuscitation is considered
adequate.
severe sepsis
corticosteroids.

33. MANAGEMENT OF SHOCK: SEPTIC SHOCK
Recombinant human activated protein C
• Decreased inflammation through reduced
levels of tnfα and nfkβ
• Decreased thrombin production leading to
anticoagulation
• Pro-fibrinolytic action through modulation
of fibrinolysis inhibitors. 21,200 COST

34. MANAGEMENT OF SHOCK:
ANAPHYLACTIC SHOCK:
Adjunctive drugs include
• H2-antagonists,
• Antihistamines,
• Corticosteroids
• Beta2-agonists
for airway symptoms.
Glucagon and noradrenaline
may be required for patients on
beta-blockers who may have
resistant severe hypotension
and bradycardia

35. MANAGEMENT OF SHOCK:
ANAPHYLACTIC SHOCK:
.

36. MANAGEMENT OF SHOCK:
NEUROGENIC SHOCK:
. • Priority focuses on airway, breathing and
circulation
• maintain a MAP >80–85 mmHg to restore spinal
cord perfusion
• Respiratory function is closely monitored to prevent
or minimise atelectasis, pneumonia and secretion
retention.

37. MANAGEMENT OF SHOCK:
NEUROGENIC SHOCK:
.• Priority focuses on airway, breathing and
circulation
• Maintain a MAP >80–85 mmhg to restore
spinal cord perfusion
• Respiratory function is closely monitored to
prevent or minimise atelectasis, pneumonia and
secretion retention.

38. Nursing diagnoses:
.
• Impaired tissue perfusion (cerebral, cardiopulmonary,
peripheral) associated with decreased cardiac output.
• Decrease in cardiac output associated with mechanical
factors (preload, afterload and myocardial contractility)
• Impaired gas exchange associated with increased
pulmonary capillary permeability