This document discusses shock, including its definition, categories, pathophysiology, and management. It defines shock as inadequate tissue perfusion to meet demands, usually due to low blood flow or oxygen delivery. The four main categories of shock are hypovolemic, cardiogenic, obstructive, and distributive. Compensatory mechanisms aim to maintain tissue perfusion through vasoconstriction and fluid retention, but failure of these mechanisms leads to end organ dysfunction. Goals of treatment are to optimize preload, contractility, afterload, and tissue oxygen delivery through volume resuscitation and vasoactive drugs.

2.  DR. Neeraj Kumar Jain
 Assistant Professor
 Deptt. Of Surgery

3.  Define shock and its different categories
 Review basic physiologic and
pathophysiologic aspects of shock

4.  Inadequate tissue perfusion to meet tissue
demands. Usually result of inadequate blood
flow and/or oxygen delivery
Circulatory failure is a life-threatening medical
condition that occurs due to inadequate substrate
for aerobic cellular respiration. In the early stages
this is generally an inadequate tissue level of
oxygen.
 Shock is not a blood pressure diagnosis

5.  In Adults:
◦ systolic BP  90 mm Hg
◦ mean arterial pressure  60 mm Hg
◦  systolic BP > 40 mm Hg from the patient’s
baseline pressure

6. Oxygen
Demand > Supply

7. • THE HEART (pump)
• THE BLOOD (circulating fluid)
• THE VASCULAR CAPACITY
(veins and arteries)
• THE MICRO- CIRCULATION

8.  Fluid
 Pump
 Vessels
 Flow

9. ATP + H2O  ADP + Pi + H+ + Energy
Acidosis results from the accumulation of acid
when during anaerobic metabolism the creation
of ATP from ADP is slowed.
H+ shift extracellularly and a metabolic acidosis
develops

10. • Cellular responses to decreased systemic oxygen
delivery
•ATP depletion → ion pump dysfunction
•Cellular edema
•Hydrolysis of cellular membranes and cellular
death
• Goal is to maintain cerebral and cardiac perfusion
•Vasoconstriction of splanchnic, musculoskeletal,
and renal blood flow
• Leads to systemic metabolic lactic acidosis that
overcomes the body’s compensatory mechanisms

11. DO2
O2
CASECADES
HEMO
DYNAMICS
VENTILATION
PULMONARY O2
EXCHANGE
O2 TRANSPORT
TISSUE EXCHANGE
QT
HB CONTENT
MICR
CIRCULATION
QT x HB x 10 x 1.36 X SO2 + PO2 x0.003

12. TISSUE PERFUSION
CONSTANT FLOW
CONSTANT DO2
TARGET FUNCTION OF CVS
REGIONAL PERFUSION
PRESSURE

13. P = F X R
Autorgulation is controlled by;
*** Myogenic *NO
*** Metabolic *H Ione
*ADENOSINE *CO2
*PG *O2
F
P
R
P R
F
F
CONSTANT
TISSUE
PERFUSION
MAP=60mmHg
Tissue perfusion

14. Large arteries Resistant
arteriole
Precapillary
arteriole
Capillary
Post capillary
venule
Collecting vein
Capacitance
vein
MAP
R
F
BP Constriction Dilatation Constant Constriction
Constriction Dilatation Constant ConstrictionBP
MAP<60 Constriction no more Flow Constriction
=
x

15. REGIONAL
PERFUSION
PRESSURE MAP
QT
SVR
MAP = QT X SVR

16. BODY RESPONSE TO SHOCK
Neuro endocrinal
Auto regulation
Aortic arch, carotid
body, cerebral
ischemia, renal
ischemia
Catecholamine
ADH, RAAS,
STEROIDS
Vasoconstriction
Salt and water
retention
To keep regional
perfusion pressure
Vasodilatation
To keep organ
flow constant
P = F X R
MAP 60 mmHg
TISSUE PERFUSION
P = F X R

17.  Oxygen content = 1.34 (Hgb x SaO2) +
(PaO2 x 0.003)
 SaO2: Oxygen saturation
 Hgb: Hemoglobin concentration
 PaO2: partial pressure Oxygen in plasma
 To improve Oxygen content
◦ Increase Hemoglobin concentration
◦ Increase saturation

18.  Cardiac output
◦ C.O. = Heart rate x stroke volume
 To improve Cardiac output
◦ Increase Heart rate
◦ Increase Stroke Volume
 Preload – volume of blood in the ventricle
 Afterload – resistance to contraction
 Contractility – force applied

19. Compensatory mechanisms for shock
1** S.V.R.
vascular
capacity
Spasm of large and
resistant arteries
Catecholamine
Vasopressin
Angiotensin 2
Cortisol
Aldosterone
2** QT
Effective
blood
volume
x =BP (MAP> 60mmHg)
*Venous spasm to V.R.
*Salt retention Aldosterone
* Water retention ADH
*Stimulation of thirst Ag.2
*Decrease hydrostatic cap .P.
Tissue fluid reabsorption at
rate 15 ml/ kg /h
Target point
Mediators

21.  Weil and Shubin in 1972 classification
 Four major categories
◦ Hypovolemic
◦ Cardiogenic
◦ Extracardiac Obstructive
◦ Distributive
 Overlap exists, and also concomitant
categories exist
TYPES OF
SHOCK

22.  Compensated
 Organ perfusion is maintained
 Uncompensated
 Circulatory failure with end organ dysfunction
 Irreverisble
◦ Irreparable loss of essential organs

23.  #1 cause of death world wide
◦ Gastroenteritis
◦ Hemorrhagic – Trauma, GI bleed

24. THE BLOOD
WHOLE
BLOOD
EXTERNAL
HG.
INTERNAL
HG.
PLASMA
GUT
*VOMITING
*NGT. DRAIN
*DIARRHOEA
* FISTULA
SKIN
•SWEAT
•* BURN
KIDNEY
*DM
*DI
*DIURETIC
3rd SPACE
* ASCITES

25. Class I Class II Class III Class IV
Blood Loss < 750 750-1500 1500-2000 > 2000
% Blood Vol. < 15% 15 – 30% 30 – 40% > 40%
Pulse < 100 > 100 > 120 > 140
Blood Pressure Normal Normal Decreased Decreased
Pulse Pressure Normal Decreased Decreased Decreased
Resp. Rate 14 – 20 20 – 30 30 – 40 > 40
UOP > 30 20 – 30 5 – 15 negligible
Mental Status sl. Anxious mildly anx confused lethargic
Fluid crystalloid crystalloid blood blood

26.  Early
◦ Increase HR
◦ Decrease perfusion
◦ Normal BP, decrease pulse pressure
 Late
◦ Sign increase HR
◦ Sign decrease perfusion
◦ Decrease BP
◦ End organ dysfunction

28. Pump failure/malfunction
(decreased contractility)

29.  Myocardial
◦ Infarction, contusion, myocarditis,
cardiomyopathy, pharmacologic, depressant
factors
 Mechanical
◦ Valvular stenosis, regrurgitation
◦ Septal Defects
 Arrhythmogenic

30. CARDIAC
CAUSESAFTERLOAD
PRELOAD
VALVES
MUSCLE POWER
RATE&
RHYTHEM

31.  Tachycardia
 Tachypnea
 Respiratory distress
 Mental status change
 Cool extremities
 Poor perfusion
 Signs of dehydration

33.  Extrinsic Vascular Compression
◦ tumors, fibrosis
 Increased Intrathoracic Pressure
◦ Tension pneumo; high autopeep in PPV
 Flow obstruction
◦ PE, Air embolism, tumors, Ao dissection, Ao
coarctation, acute pulmonary HTN, tamponade.

35. •Tension pneumothorax
•Air trapped in pleural space with 1 way valve,
air/pressure builds up
• Mediastinum shifted impeding venous return
• Chest pain, SOB, decreased breath sounds
•No tests needed!
• Rx: Needle decompression, chest tube

36. •Cardiac tamponade
•Blood in pericardial sac prevents venous return to
and contraction of heart
• Related to trauma, pericarditis, MI
• Beck’s triad: hypotension, muffled heart sounds,
JVD
• Diagnosis: large heart CXR, echo
• Rx: Pericardiocentisis

37. •Pulmonary embolism
•Virscow triad: hypercoaguable, venous injury,
venostasis
• Signs: Tachypnea, tachycardia, hypoxia
• Low risk: D-dimer
•Higher risk: CT chest or VQ scan
• Rx: Heparin, consider thrombolytics

39.  SIRS-related As sepsis (infectious);
pancreatitis; trauma; burns.
 Anaphylactic/anaphylactoid
 Spinal Trauma (low pulse, SVR low)
 Toxic, pharmacologic (B-blockers overdose)
 Endocrine (thyroid, adrenal crisis)

40.  Abnormal vessel tone
(decreased afterload)

41. Vasodilitation Venous Pooling
Decreased Afterload
Maldistribution of regional blood flow

42.  Neurogenic or Anaphylactic Shock
 Diminished or absent sympathetic tone
 Reduce peripheral vascular tone
 Peripheral pooling of blood volume
 Inadequate venous return
 Decreased perfusion, acidosis, hypotension

43. •Anaphylaxis – a severe systemic
hypersensitivity reaction characterized
by multisystem involvement
•IgE mediated
•Anaphylactoid reaction – clinically
indistinguishable from anaphylaxis, do
not require a sensitizing exposure
•Not IgE mediated

44. •What are some symptoms of anaphylaxis?
• First- Pruritus, flushing, urticaria appear
•Next- Throat fullness, anxiety, chest tightness,
shortness of breath and lightheadedness
•Finally- Altered mental status, respiratory
distress and circulatory collapse

45. • Risk factors for fatal anaphylaxis
• Poorly controlled asthma
• Previous anaphylaxis
• Reoccurrence rates
• 40-60% for insect stings
• 20-40% for radiocontrast agents
• 10-20% for penicillin
• Most common causes
• Antibiotics
• Insects
• Food

46. • Mild, localized urticaria can progress to full
anaphylaxis
• Symptoms usually begin within 60 minutes of
exposure
• Faster the onset of symptoms = more severe reaction
• Biphasic phenomenon occurs in up to 20% of patients
• Symptoms return 3-4 hours after initial reaction has cleared
• A “lump in my throat” and “hoarseness” heralds life-
threatening laryngeal edema

47. •Clinical diagnosis
•Defined by airway compromise,
hypotension, or involvement of cutaneous,
respiratory, or GI systems
•Look for exposure to drug, food, or
insect
•Labs have no role

48. •Occurs after acute spinal cord injury
•Sympathetic outflow is disrupted leaving
unopposed vagal tone
•Results in hypotension and bradycardia
•Spinal shock- temporary loss of spinal
reflex activity below a total or near total
spinal cord injury (not the same as
neurogenic shock, the terms are not
interchangeable)

49. •Loss of sympathetic tone results in warm and
dry skin
•Shock usually lasts from 1 to 3 weeks
•Any injury above T1 can disrupt the entire
sympathetic system
• Higher injuries = worse paralysis

50.  Terminology in Sepsis
◦ Infection = response to micro organism
◦ Bacteremia = bug in blood
◦ Systemic Inflammatory Response Syndrome (SIRS)
 T>38, <36
 Increase HR
 Increase RR, paCO2<32
 WBC>12,000, <4,000, >10% bands

51.  Terminology in Sepsis
◦ Sepsis = SIRS (systemic inflammatory response
syndrome) as response to a known infection
◦ Severe sepsis = Sepsis + organ dysfunction
◦ Septic Shock = Sepsis + inadequate oxygen delivery
◦ Multiple Organ Dysfunction Syndrome (MODS) –
organ dysfunction that requires intervention

52.  Components of Septic shock
◦ Decreased volume
◦ Decreased pump function
◦ Abnormal vessel tone

53.  Therapy for Caridovascular Support
Preload Volume
Contractility Inotropes
Afterload Vasodilators

54. Etiologies
 Inflammatory: too much, too little
 Coagulation pathway: DIC-bleeding, pro-
coagulant, microthombosis
 Multiple organ system failure

55.  Early – warm shock – similar to neurogenic
shock
 Late – Cold shock – similar to cardiogenic
shock

56. Early Late
Heart rate Tachycardia Tachycardia/
bradycardia
Blood pressure Normal decreased
Peripheral
Perfusion
Warm/cool
Dec./inc. pulses
Cool
Dec. pulses

57. Early Late
End-organ: skin Dec. cap refill Very dec. cap
Refill
Brain Irritable,
restless
Lethargic,
unresponsive
Kidneys Oliguria Oliguria, anuria

58. HYPOXIC
FAILURE
COMPENSATORY
POST CAP.VASO-CON.
STRESS
PRE&POST CAP.V.CON.
PRECAPILLARY SHUNT
FAILURE
OPEN PRECAP
LEAKAGE
RECOVARY

59. Type PAOP C.O. SVR
(pul. Art.occul. Press.)
HYPOVOLEMIC   
CARDIOGENIC   
DISTRIBUTIVE  or N varies 
OBSTRUCTIVE   

60. SEQULEE OF SHOCK
INSULT
MILD Within the adaptive mechanisms
Moderate
To severe
Beyond the adaptive mechanisms
Normal physiologic
oscillation
Pathological
oscillation
Failure of
compensatory
mechanisms
MAP<60
Failure of
Autorgulation
Tissue flow
DO2
CEF OF O2
Tissue necrosisMSODDeath

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