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Shock basic
1.
2. ď˝ DR. Neeraj Kumar Jain
ď˝ Assistant Professor
ď˝ Deptt. Of Surgery
3. ď˝ Define shock and its different categories
ď˝ Review basic physiologic and
pathophysiologic aspects of shock
4. ď˝ 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.
ď˝ Shock is not a blood pressure diagnosis
5. ď˝ In Adults:
⌠systolic BP ďŁ 90 mm Hg
⌠mean arterial pressure ďŁ 60 mm Hg
âŚ ď˛ systolic BP > 40 mm Hg from the patientâs
baseline pressure
9. ATP + H2O ď 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
â˘ATP depletion â ion pump dysfunction
â˘Cellular edema
â˘Hydrolysis of cellular membranes and cellular
death
⢠Goal is to maintain cerebral and cardiac perfusion
â˘Vasoconstriction of splanchnic, musculoskeletal,
and renal blood flow
⢠Leads to systemic metabolic lactic acidosis that
overcomes the bodyâs compensatory mechanisms
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
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. ď˝ Oxygen content = 1.34 (Hgb x SaO2) +
(PaO2 x 0.003)
ď§ SaO2: Oxygen saturation
ď§ Hgb: Hemoglobin concentration
ď§ PaO2: partial pressure Oxygen in plasma
ď˝ To improve Oxygen content
⌠Increase Hemoglobin concentration
⌠Increase saturation
18. ď˝ Cardiac output
⌠C.O. = Heart rate x stroke volume
ď˝ To improve Cardiac output
⌠Increase Heart rate
⌠Increase Stroke Volume
ď Preload â volume of blood in the ventricle
ď Afterload â resistance to contraction
ď Contractility â 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
20.
21. ď˝ Weil and Shubin in 1972 classification
ď˝ Four major categories
⌠Hypovolemic
⌠Cardiogenic
⌠Extracardiac Obstructive
⌠Distributive
ď˝ Overlap exists, and also concomitant
categories exist
TYPES OF
SHOCK
22. ď˝ Compensated
ď Organ perfusion is maintained
ď˝ Uncompensated
ď Circulatory failure with end organ dysfunction
ď˝ Irreverisble
⌠Irreparable loss of essential organs
23. ď˝ #1 cause of death world wide
⌠Gastroenteritis
⌠Hemorrhagic â Trauma, GI bleed
33. ď˝ Extrinsic Vascular Compression
⌠tumors, fibrosis
ď˝ Increased Intrathoracic Pressure
⌠Tension pneumo; high autopeep in PPV
ď˝ Flow obstruction
⌠PE, Air embolism, tumors, Ao dissection, Ao
coarctation, acute pulmonary HTN, tamponade.
34.
35. â˘Tension pneumothorax
â˘Air trapped in pleural space with 1 way valve,
air/pressure builds up
⢠Mediastinum shifted impeding venous return
⢠Chest pain, SOB, decreased breath sounds
â˘No tests needed!
⢠Rx: Needle decompression, chest tube
36. â˘Cardiac tamponade
â˘Blood in pericardial sac prevents venous return to
and contraction of heart
⢠Related to trauma, pericarditis, MI
⢠Beckâs triad: hypotension, muffled heart sounds,
JVD
⢠Diagnosis: large heart CXR, echo
⢠Rx: Pericardiocentisis
42. ď˝ Neurogenic or Anaphylactic Shock
ď˝ Diminished or absent sympathetic tone
ď˝ Reduce peripheral vascular tone
ď˝ Peripheral pooling of blood volume
ď˝ Inadequate venous return
ď˝ Decreased perfusion, acidosis, hypotension
43. â˘Anaphylaxis â a severe systemic
hypersensitivity reaction characterized
by multisystem involvement
â˘IgE mediated
â˘Anaphylactoid reaction â clinically
indistinguishable from anaphylaxis, do
not require a sensitizing exposure
â˘Not IgE mediated
44. â˘What are some symptoms of anaphylaxis?
⢠First- Pruritus, flushing, urticaria appear
â˘Next- Throat fullness, anxiety, chest tightness,
shortness of breath and lightheadedness
â˘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 âlump in my throatâ and âhoarsenessâ heralds life-
threatening laryngeal edema
47. â˘Clinical diagnosis
â˘Defined by airway compromise,
hypotension, or involvement of cutaneous,
respiratory, or GI systems
â˘Look for exposure to drug, food, or
insect
â˘Labs have no role
48. â˘Occurs after acute spinal cord injury
â˘Sympathetic outflow is disrupted leaving
unopposed vagal tone
â˘Results in hypotension and bradycardia
â˘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. â˘Loss of sympathetic tone results in warm and
dry skin
â˘Shock usually lasts from 1 to 3 weeks
â˘Any injury above T1 can disrupt the entire
sympathetic system
⢠Higher injuries = worse paralysis
51. ď˝ 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) â
organ dysfunction that requires intervention
52. ď˝ Components of Septic shock
⌠Decreased volume
⌠Decreased pump function
⌠Abnormal vessel tone
53. ď˝ Therapy for Caridovascular Support
Preload Volume
Contractility Inotropes
Afterload Vasodilators
54. Etiologies
ď˝ Inflammatory: too much, too little
ď˝ Coagulation pathway: DIC-bleeding, pro-
coagulant, microthombosis
ď˝ Multiple organ system failure
55. ď˝ Early â warm shock â similar to neurogenic
shock
ď˝ Late â Cold shock â 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
59. Type PAOP C.O. SVR
(pul. Art.occul. Press.)
HYPOVOLEMIC ďŻ ďŻ ď
CARDIOGENIC ď ďŻ ď
DISTRIBUTIVE ďŻ or N varies ďŻ
OBSTRUCTIVE ď ďŻ ď
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