1. Shock is defined as a state of low tissue perfusion resulting from inadequate oxygen and glucose delivery to cells. This causes cells to switch from aerobic to anaerobic metabolism, leading to cell death if not corrected. 2. The pathophysiology of shock involves simultaneous cellular, microvascular, and systemic changes including metabolic acidosis, organ ischemia, immune system activation, and sympathetic nervous system response. 3. Shock is classified based on its underlying cause as hypovolemic, cardiogenic, obstructive, distributive, or endocrine. Resuscitation priorities include addressing hypovolaemia with intravenous fluids before considering further treatment.

1. MARMAGHAT (SHOCK)
Dr. Alok Kumar
PhD Shalya Tantra
NEIAH, Shillong

2. Samanya lakshana of marmaghata
देहप्रसुप्तिर्ुुरुिा सम्मोहः शीिकाममिा| स्वेदो मूर्च्ाु वममः श्वासो ममुववद्धस्य
लक्षणम्|| A.S. Sa. 7/47
Numbness , spasm/heaviness, confusion/ nervousness, thirst, sweating,
unconsciousness, vomiting, dyspnea are the common features of
marmaghata.

3. भ्रमः प्रलापः पिनं प्रमोहो ववचेष्टनं संलयनोष्णिे च |
स्रस्िाङ्र्िा मूर्च्ुनमूर्धवुवािस्िीव्रा रुजो वािकृ िाश्च िास्िाः ||३४||
मांसोदकाभं रुधधरं च र्र्च्ेि् सवेप्रियार्थोपरमस्िर्थैव |
दशाधुसङ््येष्ववप ववक्षिेषु सामारयिो ममुसु मलङ्र्मुक्िम् ||३५||
Su.Su 25/34-35
देहस्य रुधधरं मूलं रुधधरेणैव धायुिे |
िस्माद्यत्नेन संरक्ष्यं रक्िं जीव इति प्स्र्थतिः ||४४|| Su.Su 14/44

4. 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.

5. Pathophysiological Events
All theses event happens simultaneously….
1. Cellular
2. Micro-vascular
3. Systemic

6. Cellular
Cells run-down with oxygen and glucose
Aerobic respiration turns to Anaerobic
Collection of lactic acid lead to metabolic acidosis
As glucose exhausted respiration ceases
Sodium potassium pump stop
Intracellular lysosomes release autodigestive enzymes and cell lysis ensues
Intracellular contents, including potassium, are released into the bloodstream.

7. Micro-vascular
As tissue ischemia progresses, changes in the local environment
activation of the immune and coagulation systems
generation of oxygen free radicals and cytokine release
injury of the capillary endothelial cells.
Damaged endothelium loses its integrity and becomes ‘leaky’
Spaces between endothelial cells allow fluid to leak out and tissue oedema ensues,
worsening cellular hypoxia

8. Systemic
These system take active participation in shock
•Cardiovascular
•Respiratory
•Renal
•Endocrine

9. Cardiovascular
As preload and afterload decrease
Compensatory baroreceptor response resulting in increased
sympathetic activity and release of catecholamines into the
circulation.
This results in tachycardia and systemic vasoconstriction
(except in sepsis).

10. Respiratory
The metabolic acidosis and increased sympathetic response
Increased respiratory rate and tiny ventilation
Leads to increase the excretion of carbon dioxide
(and so produce a compensatory respiratory alkalosis).

11. Renal
Decreased perfusion pressure in the kidney
Leads to reduced filtration at the glomerulus
Resulting decreased urine output.
The renin–angiotensin–aldosterone axis is stimulated
Resulting in further vasoconstriction and increased sodium and water
reabsorption by the kidney

12. Endocrine
As well as activation of the adrenal and renin–angiotensin systems
Vasopressin (antidiuretic hormone) is released from the hypothalamus in
response to decreased preload and results in vasoconstriction and
reabsorption of water in the renal collecting system.
Cortisol is also released from the adrenal cortex, contributing to the
sodium and water reabsorption and sensitizing the cells to
catecholamines

13. Ischaemia–reperfusion syndrome
Tissue damage due to Hypoxia & local inflammation
Normal circulation is restored
The acid and potassium recirculate in body
Can lead to direct myocardial depression, vascular dilatation and
further hypotension

14. The cellular and humoral elements activated by the hypoxia
(complement, neutrophils, micro-vascular thrombi) are flushed back
into the circulation
They causes further endothelial injury to organs such as the lungs
and kidneys
This leads to acute lung injury, acute renal injury, multiple organ
failure and death.

15. How to avoid ????
Reducing the extent and duration of tissue hypo-perfusion.

16. Classification of shock (HODEC)
There are various classification of shock but most
clinical approachable is on the basis of initiating
mechanism
•Hypovolemic
•Obstructive
•Distributive
•Endocrine
•Cardiogenic

18. Hypovolemic
Caused by a reduced circulating volume May be:
Hemorrhagic
Non-hemorrhagic (dehydration, excessive fluid loss by diarrheoa,
vomiting, urinary or fluid in third space i.e. exudation)
Hypovolemia is probably the most common form of shock and is to
some degree a component of all other forms of shock. Absolute or
relative hypovolemia must be excluded or treated in the
management of the shocked state, regardless of cause.

19. Cardiogenic shock
Failure of the heart to pump blood to the tissues.
Causes
Myocardial infarction, cardiac dysrhythmias, valvular heart disease,
blunt myocardial injury and cardiomyopathy.
Cardiac insufficiency may also be caused by myocardial depression
resulting from endogenous factor like (e.g. bacterial and humoral
agents released in sepsis) or exogenous factors, such as
pharmaceutical agents or drug abuse.
Evidence of venous hypertension with pulmonary or systemic oedema
may coexist with the classic signs of shock.

20. Obstructive shock
In obstructive shock there is a reduction in preload because of
mechanical obstruction of cardiac filling.
Cardiac tamponade, tension pneumothorax, massive pulmonary
embolus and air embolus. In each case there is reduced filling of the
left and/or right sides of the heart leading to reduced preload and a
fall in cardiac output

21. Distributive shock
Inadequate organ perfusion is complemented by vascular dilatation
with hypotension, low systemic vascular resistance, inadequate
afterload and a resulting abnormally high cardiac output.
Present in
• Anaphylaxis
• Septicemia ( septic shock)
• Spinal cord injury

22. Endocrine shock
Endocrine shock may present as a combination of hypovolaemic,
cardiogenic and distributive shock.
Causes of endocrine shock include hypo- and hyperthyroidism and
adrenal insufficiency.
Hypothyroidism causes a shock result of disordered vascular and cardiac
responsiveness to circulating catecholamines. Cardiac output falls
because of low inotropy and bradycardia. There may also be an
associated cardiomyopathy.
Thyrotoxicosis may cause a high-output cardiac failure.

23. Adrenal insufficiency leads to shock as a result of hypovolaemia
and a poor response to circulating and exogenous catecholamines.
Adrenal insufficiency may result from pre-existing Addison’s
disease or it may be a relative insufficiency caused by a pathological
disease state such as systemic sepsis.

24. Severity of shock
•Compensated shock
•De-compensated
•Mild shock
•Moderate shock
•Severe shock

25. Compensated shock
Apart from a tachycardia and cool peripheries (vasoconstriction, circulating
catecholamines) there may be no other clinical signs of hypovolaemia.
This condition is occult tissue perfusion this state will lead to multiple organ failure
and death if prolonged because of the ischaemia–reperfusion effect.
Patients with occult hypo-perfusion (metabolic acidosis despite normal urine
output and cardiorespiratory vital signs) for more than 12 hours have a
significantly higher mortality rate, infection rate and incidence of multiple organ
failure.
In general, loss of around 15% of the circulating blood volume is within normal
compensatory mechanisms.
Kidneys
Lungs
Brain
Skin
Muscle
Gastrointestinal tract.

26. De-compensation
Further loss of circulating volume overloads the body’s
compensatory mechanisms and there is progressive renal,
respiratory and cardiovascular de-compensation.
Blood pressure is usually well maintained and only falls after
30–40% of the circulating volume has been lost.

27. Mild shock
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 distributive
shock).

28. Moderate shock
As shock progresses, renal compensatory mechanisms
fail, renal perfusion falls and urine output dips below
0.5mlkg–1h–1.
There is further tachycardia and now the blood pressure
starts to fall.
Patients become drowsy and mildly confused.

29. Severe shock
In severe shock there is profound tachycardia and
hypotension.
Urine output falls to zero and patients are
unconscious with laboured respiration.

30. Clinical feature Compensated Mild Moderate Severe
Lactic acidosis + ++ ++ +++
Urine output Normal Normal Reduced Anuric
Level of
consciousness
Normal Mild anxiety Drowsy Comatose
Respiratory
rate
Normal Increased Increased Laboured
Pulse rate Normal Increased Increased Increased
Blood pressure Normal Normal Mild
hypotension
Severe
hypotension
Clinical feature of shock

31. Pitfalls
The problem is that all these classical sign symptoms are not present in every patient.
Patient may have shock despite the absence of these classical sign.
1. Capillary refill
2. Tachycardia
3. Blood pressure

32. Consequences
1. Un-resuscitatable shock
2. Multiple organ failure

33. RESUSCITATION
Resuscitation should not be delayed in order to definitively diagnosis…
1. The timing and nature of resuscitation will depend on the type of shock and the
timing and severity of the insult.
2. 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.
3. 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.
4. If patient is actively loosing blood, operative haemorrhage control should not be
delayed and resuscitation should proceed in parallel with surgery. If patient not
loosing blood actively then must be resuscitated before underwent surgery. For eg in
bowel obstruction leading shock patient must resuscitated before surgery.

34. Fluid therapy
1. In all cases of shock, regardless of classification, hypovolaemia and inadequate
preload must be addressed before other therapy is instituted.
2. Therefore, First-line therapy is intravenous access and administration of
intravenous fluids.
3. Access should be through short, wide-bore catheters that allow rapid infusion of
fluids as necessary.

35. Type of fluids
1. Blood
2. Crystalloid ( Normal saline, Ringer’s lactate, Hartmann’s solution)
3. Colloid (albumin or commercially available products)

36. Dynamic fluid response
The shock status can be determined dynamically by the cardiovascular
response to the rapid administration of a fluid bolus. The 250-500 ml fluid
should be given in first 5-10 minute and the response of therapy must be
observed in term of-
1. Heart Rate
2. Blood Pressure
3. Central Venous Pressure (CVP)
Patients can be divided into ‘responders’, ‘transient responders’ and
‘non-responders’.

37. Responders
1. Severely volume
depleted and are likely
to have major on-
going loss of
intravascular volume,
usually through
persistent
uncontrolled
haemorrhage.
1. Improvement but
then revert to their
previous state over
the next 10–20min.
2. These patients
have moderate on-
going fluid losses
1. Improvement in
their cardiovascular
status, which is
sustained.
2. These patients are
not actively losing
fluid but require
filling to a normal
volume status
Non-
responders
Transient
responders

38. Vasopressor and inotropic support
Not included in first line therapy for shock..
1. Vasopressor agents (phenylephrine, noradrenaline) are
indicated in distributive shock states.
2. 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.

39. Monitoring
Minimum
■ Electrocardiogram ■ Pulse oximetry ■ Blood pressure
■ Urine output
Additional modalities
■ Central venous pressure ■ Invasive blood pressure ■
Cardiac output ■ Base deficit and serum lactate

40. Endpoints of resuscitation
1. Traditionally patients have been resuscitated until they
have a normal pulse, blood pressure and urine output.
2. Resuscitation algorithms directed at correcting global
perfusion endpoints are base deficit, lactate, mixed
venous oxygen saturation.