This document provides an overview of shock, including its history, definition, pathogenesis, stages, classification, and treatment. It discusses the various types of shock - hypovolemic (hemorrhagic), cardiogenic, obstructive, and distributive (septic, anaphylactic, neurogenic). For hypovolemic shock, it outlines the stages, compensatory mechanisms, assessment including vital signs and labs, and classification based on percentage of blood loss. Treatment of hypovolemic shock involves initial and late resuscitation, with goals of hemodynamic stabilization while avoiding over-resuscitation and permissive hypotension when possible.

1. SHOCK
DR. KANIKA CHAUDHARY
1

2. 2
OVERVIEW
• HISTORY
• DEFINITION
• PATHOGENESIS AND ORGAN RESPONSE
• STAGES OF SHOCK
• CLASSIFICATION
• HYPOVOLEMIC SHOCK:-
 HEMORRHAGIC SHOCK
• CARDIOGENIC SHOCK
• OBSTRUCTIVE SHOCK
• DISTRIBUTIVE SHOCK:-
 SEPTIC SHOCK
 ANAPHYLATIC SHOCK
 NEUROGENIC SHOCK
• REFERENCES

3. HISTORY
• Despite recognition of a post traumatic syndrome by Greek physicians
such as Hippocrates and Galen, the origin of the term shock is generally
credited to the French surgeon Henri Francois Le Dran, who in 1737
defined the same as “A treatise of reflections drawn from experience with
gunshot wounds” and coined the term “choc” to indicate a severe impact .
• An inappropriate translation by the English physician Clare, in 1743, led
to the introduction of the word “shock” to the English language to indicate
the sudden deterioration of a patient’s condition when major trauma has
occurred.
3

4. • “The state in which profound and wide spread reduction of effective perfusion
leads first to reversible, and then, if prolonged, to irreversible cellular injury –
IJA,Shock review ,2003
• Shock is characterized by systemic hypoperfusion of tissues; it can be caused
by diminished cardiac output or by reduced effective circulating blood volume.
The consequences are impaired tissue perfusion and cellular hypoxia –Robbin’s basic
pathology 9th ed
• Shock is the clinical syndrome that results from inadequate tissue perfusion-
Harrison’s 19th ed
DEFINITION
4

5. 5
PATHOGENESIS AND ORGAN RESPONSE
1. CELLULAR RESPONSE:-
Inadequate tissue perfusion
Reduced amount of both oxygen and substrate
Shift from aerobic to anerobic metabolism
Lactic acid accumulation , fall in pH metabolic acidosis
Cell membrane dysfunction and associated increase in intracellular sodium and water

6. 6
Swelling of mitochondria and other intracellular organelles including lysosomes
If this process continues cell membranes break down and enzymes are released, causing
destruction of the cell and local tissue damage
Proteolytic enzymes released from damaged cells initiate formation of plasma kinins,
activation of intravascular coagulation and activation of complement
Kinins increase capillary permeability, dilate small blood vessels and depress myocardial
function

7. 7
2. MICROCIRCULATION:-
• Innervated by the sympathetic nervous system and has a profound effect on the
larger arterioles. Following hemorrhage, larger arterioles vasoconstrict;
however, in sepsis or neurogenic shock, these vessels vasodilate
• Vasopressin, angiotensin II, and endothelin-1, also lead to vasoconstriction to
limit organ perfusion to organs such as skin, skeletal muscle, kidneys, and the
gastrointestinal (GI) tract to preserve perfusion of the myocardium and CNS
• Impairment of the microcirculation derangement of cellular metabolism
organ failure

8. 8
• Failure of the integrity of the endothelium of the microcirculation
capillary leakintracellular swelling the development of an
extracellular fluid deficitdecreased capillary hydrostatic pressure
loss of extracellular fluid volume
• Capillary dysfunction also occurs secondary to activation of endothelial
cells by circulating inflammatory mediators generated in septic shock
exacerbates endothelial cell swelling and capillary leak, as well as
increases leukocyte adherencecapillary occlusion

9. 9
3. NEUROENDOCRINE RESPONSE:-
• Hypotension disinhibits the vasomotor center increased adrenergic
output and reduced vagal activity.
• Release of norepinephrine peripheral and splanchnic vasoconstriction
• Reduced vagal activity increases the heart rate and cardiac output
• Loss of vagal activity  upregulate the innate immune inflammatory
response
• Epinephrine increased glycogenolysis and gluconeogenesis and reduced
insulin release

10. 10
4. CARDIOVASCULAR RESPONSE
Hypovolemia
Decreased ventricular preload  decreased stroke volume
Increased catecholamine release from adrenal medulla
Increased heart rate and contractility

11. 11
5. PULMONARY RESPONSE:-
• Stimulation of pulmonary J receptors and carotid body chemoreceptors,
hypo-perfusion of the medullary respiratory center increased minute
volume (tachypnea, hyperpnea), hypocapnia and primary respiratory
alkalosis.
• Increased minute volume and decreased cardiac output  increased V/Q
ratio
• With increased workload, respiratory and diaphragmatic muscle
impairment caused by hypoperfusion respiratory failure. If shock is not
promptly reversed and the initiating condition controlled adult respiratory
distress syndrome (ARDS) may develop

12. 12
6. RENAL RESPONSE:-
Hypoperfusion
Decreased renal blood flow, particularly blood flow to cortex
Activation of RAAS
Aldosterone release by adrenal cortex and vasopressin by posterior pituitary
Reduced GFR +increased aldosterone and vasopressin= OLIGURIA

13. 13
• The net effect is a decreased glomerular filtration rate. The three pathologic changes
seen are
(a) Tubular necrosis
(b) Tubular obstruction by casts or debris and
(c) Tubular epithelial damage

14. 14
7. GASTROINTESTINAL:-
• Ileus, erosive gastritis,pancreatitis, acalculous cholecystitis and colonic submucosal
hemorrhage
• Enteric bacteria and antigens translocate from the gut lumen into the systemic circulation
during gut ischemia causing irreversible shock
8. LIVER:-
• Centrilobular injury with mild increases of transaminases and lactate dehydrogenases
usually peaks in 1-3 days of ischemic insult and resolves over 3-10 days
• Shock liver associated with massive ischemic necrosis and a major elevation of
transaminases is atypical in the absence of extensive hepatocellular disease

15. 15
9. HEMATOLOGICAL DISTURBANCES:-
Trigger
Coagulation activation
Intravascular coagulation
Consumption of clotting factors
& platelets
Fibrin deposition
Fibrinolysis
Fibrin degradation
products
HAEMORRHAGE
Microvascular thrombosis
ORGAN DYSFUNCTION

16. 16
10. METABOLIC DISTURBANCES:-
• Disruption of the normal cycles of carbohydrate, lipid, and protein metabolism
• Anaerobic metabolism lactate
• Increased hepatic gluconeogenesis
• Hepatic lipogenesis Increased Triglycerides
• Protein catabolism Muscle wasting

17. 17
11. INFLAMMATORY RESPONSES:-

18. 18
STAGES OF SHOCK
• An initial nonprogressive stage, during which reflex compensatory
mechanisms are activated and vital organ perfusion is maintained
• A progressive stage, characterized by tissue hypoperfusion and onset of
worsening circulatory and metabolic derangement, including acidosis
• An irreversible stage, in which cellular and tissue injury is so severe that
even if the hemodynamic defects are corrected, survival is not possible

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NON PROGRESSIVE SHOCK
COMPENSATORY MECHANISM
1.Baroreceptor reflexes sympathetic stimulation of the circulation.
2.Central nervous system ischemic response:-Not activated significantly until the arterial
pressure falls below 50 mm Hg.
3.Reverse stress-relaxation of the circulatory system, which causes the blood vessels to
contract around the diminished blood volume so that the blood volume that is available more
adequately fills the circulation
4.Increased secretion of renin by the kidneys and formation of angiotensinII,
constricts the peripheral arteries and decreased output of water and salt by the kidneys

20. 20
5.Increased secretion by the posteriorpituitary vasopressinconstricts the
peripheral arteries and veins and increases water retention by the kidneys
6.Increased secretion by the adrenalmedulla of epinephrine and
norepinephrine constricts the peripheral arteries and veins and increases the
heart rate
7.Compensatorymechanisms that return the bloodvolume back toward
normal:-absorption of large quantities of fluid from the intestinal tract,
absorption of fluid into the blood capillaries from the interstitial spaces of the
body

21. 21
PROGRESSIVE SHOCK

22. CLASSIFICATION
• A classification based on cardiovascular characteristics, which was initially
proposed in 1972 by Hinshaw and Cox, is the most accepted one amongst
many others that have been given.
• Four major categories:
1. Hypovolemic shock
2. Cardiogenic shock
3. Obstructive shock
4. Distributive shock
22

23. 1.Hypovolemic Shock:-
• loss in circulatory volume decreased venous return, decreased filling of the
cardiac chambers decreased cardiac output
• The haemodynamic profile on monitoring of flow pressure variables shows
 low central venous pressure (CVP)
 low pulmonary capillary wedge pressure (PCWP)
 low cardiac output (CO) and cardiac index (CI) and high SVR
 The arterial blood pressure may be normal or low
23

24. 24
CAUSES:-

25. Baskett’s
Classification of Hemorrhagic Shock
CLASS I CLASS II CLASS III CLASS IV
BloodLoss (ml)
%
<750
15%
750-1500
15%-30%
1500-2000
30-40%
>2000
>40%
HR <100 >100 >120 >140
BP normal normal decrease decrease
PP normal decrease decrease decrease
RR 15-20 20-30 30-40 >35
UOP >30 20-30 5-15 negligible
CNS Normal mildly
anxious
anxious
confused
confused
lethargic
25
Baskett PJ. ABC of major trauma. Management of hypovolaemic shock. BMJ. 1990;300;1453-1457.

26. Stages of Shock - Events

27. 27
ASSESSMENT IN HEMORRHAGIC SHOCK
INITIALASSESSMENT:-
 Mentation
 Skin perfusion
 Pulse
 Blood pressure
 Pulse pressure
 Shock index
 ROPE
 Urine output
INVESTIGATION:-
 Hb
 HCT
 pH
 Serum lactate
 Base deficit
 Others

28. 28
INITIALASSESSMENT
 Changing mentation is an indicator of perfusion, it is affected by drugs, alcohol,head injury
 Pulse:-
• lacks specificity alone,
• Pulse & character together are more reliable
• “Any patient who is cool and tachycardic is in shock until proven otherwise”(ATLS)
• Relative bradycardia (paradoxical bradycardia):- pulse<90/min with SBP
<90mmhg,occurs in 45% of all hypotensive trauma
 Skin perfusion:- pale, cool, mottled(vasoconstriction)
 Capillary refill:- unreliable to measure, normal: <2 sec

29. BP Estimation from Pulse
60
70
80
80
• If you can palpate
this pulse, you
know approximately
the SBP
29

30. 30
 Systolic BP drop a late signt
 olic BP does not fall until:
• Adults 30% blood loss
• Pediatrics 40-45% blood loss
 SBP < 90 mm Hg: mortality approaches 65%
 Narrow pulse pressure suggest significant blood loss- results from increased diastolic
blood pressure from compensatory increase in catecholamine release
 Shock index(SI) = HR / SBP
i Elevated early in shock
ii Normal 0.5 - 0.7
iii SI > 0.9 predicts:
1. Acute hypovolemia in presence of normal HR & BP
2.Marker of injury, severity & mortality

31. 31
ROPE
ROPE* : Pulse Rate over Pulse Pressure Evaluation
as a method of predicting decompensation in patients
with compensated haemorrhagic shock.
PULSE RATE ÷ PULSE PRESSURE
A ROPE value of >3.0 had a positive predictive
value of < 3.0 had a negative predictive
for the development of decompensated shock**.
**Campbell, Roderick MBChB; Ardagh, Michael W. PhD; Than, Martin MBBS: Validation of the pulse rate over pressure evaluation index as a detector of
early occult hemorrhage: A prospective observational study:, Journal of Trauma and Acute Care Surgery: July 2012 –vol.73-issue1-p286-288
*Michael W Ardagh, Timothy Hodgson et al., Pulse rate over pressure evaluation (ROPE) is useful in the assessment of compensated haemorrhagic shock:
Emergency Medicine (2001) 13, 43–46

32. 32
Hemoglobin / Hematocrit
• Unreliable estimation acute blood loss
• Lag time of several hours
• Baseline value for comparison only
Hemoglobin — is not a good indicator of the depth of hemorrhage, because it
expresses a concentration of red cells, which will not change in a patient who is
losing whole blood.
Haematocrit – During loss of whole blood the proportion of RBC to plasma volume
remains unchanged.

33. 33
Arterial pH
Acidosis - Serum pH < 7.20
Ongoing Marker of Severe Physiologic Derangement
• Decreased cardiac contractility
• Decreased cardiac output
• Vasodilation and decreased BP
• Decreased hepatic and renal blood flow

34. 34
Base Deficit
Sensitive measure of inadequate perfusion
Normal range -3 to +3
Worsening BD:
◦ Inadequate volume replacement
It is a reliable marker for shock and the need for transfusion.

35. 35
Lactate
 Indirect marker of tissue hypoperfusion, cellular oxygen debt and severity
of hemorrhagic shock
 Normal value= 0.56-1.39 mmol/L
 Lactate value>5 indicative of increased mortality

36. 36
 Traditional measurement of platelets, international normalized ratio, and
partial thromboplastin time may not reflect the coagulopathy of trauma or
response to therapy effectively
 Recently, thrombo- elastography (TEG) has been used as a quicker, more
comprehensive determination of coagulopathy and fibrinolysis in the
injured patient
Others:-

37. 37
TREATMENT…..

38. 38
Class 1 Class 2 Class 3 Class 4
Blood loss(ml) UPTO 750 750-1500 1500-2000 >2000
Blood loss
(%blood volume)
UPTO 15% 15-30% 30-40% >40%
Pulse rate <100 >100 >120 >140
Blood pressure NORMAL NORMAL DECREASED DECREASED
Pulse pressure NORMAL OR ↑ DECREASED DECREASED DECREASED
Respiratory rate 14-20 20-30 30-40 >35
Urine
output(ml/hr)
>30 20-30 5-15 NEGLIGIBLE
CNS/Mental status SLIGHTLY
ANXIOUS
MILDLY
ANXIOUS
ANXIOUS
CONFUSED
CONFUSED
LETHARGIC
Fluid replacement CRYSTALLOID CRYSTALLOID CRYSTALLOID
& BLOOD
CRYSTALLOID
& BLOOD
Baskett PJ. ABC of major trauma. Management of hypovolaemic shock. BMJ. 1990;300;1453-1457.

39. 39
INITIAL RESUSCITATION….

40. 40
Resuscitation should be considered in the following two phases:
• Early: While active bleeding is still ongoing
• Late: Once all hemorrhage has been controlled

41. 41

42. 42

43. 43
HEMOSTATIC RESUSCITATION….

44. 44

45. 45

46. 46

47. 47

48. 48
•Assess for coagulopathy early
•Control bleeding and follow A,B,C protocol.
•LR is fluid of choice in trauma
•If cross matched blood is available it should be used as a initial
resuscitation fluid.
•Haemostatic resuscitation is at 1: 1: 1 ratio (PRBC: FFP: PLATELET).
•Avoid aggressive resuscitation and maintain Permissive Hypotension.
•Serial sampling of ABG and lactate level and correct acidosis.
•Start appropriate antibiotics, adequate analgesia, and early repair of
injury.

49. 49
2. CARDIOGENIC SHOCK
• Cardiogenic shock (CS) is a state of end-organ hypoperfusion due to acute catastrophic
failure of left ventricular pump function
• The definition of CS (AHA) includes hemodynamic parameters:
i. Persistent hypotension (systolic blood pressure <80 to 90 mm Hg or mean arterial
pressure 30 mm Hg lower than baseline)
ii. Severe reduction in cardiac index (<1.8 L · min−1 · m−2 without support or <2.0 to 2.2
L · min−1 · m−2 with support)
iii. Adequate or elevated filling pressure (eg, left ventricular [LV] end-diastolic pressure
>18 mm Hg or right ventricular [RV] end-diastolic pressure >10 to 15 mm Hg).

50. 50
CAUSES:-

51. 51
PATHOPHYSIOLOGY OF CARDIOGENIC SHOCK

52. 52
DIAGNOSIS:-
• Due to the unstable condition of these patients, supportive therapy must be
initiated simultaneously with diagnostic evaluation
• A focused history and physical examination should be performed, blood
specimens sent to the laboratory, and an electrocardiogram (ECG) and chest
x-ray obtained

53. 53
CLINICAL FEATURES:-
• Dyspnea
• Pale, apprehensive, and diaphoretic, and mental status may be altered
• Pulse is weak and rapid, 90–110 beats/min, or severe bradycardia due to high-grade heart
block may be present
• Systolic BP is reduced (<90 mmHg or ≥30 mmHg below baseline) with a narrow pulse
pressure (<30 mmHg)
• Tachypnea, and jugular venous distention may be present
• Acute, severe MR and VSR usually are associated with characteristic systolic murmurs
Rales are audible in most patients with LV failure

54. 54
INVESTIGATIONS:-
1. Laboratory findings:-
• WBC is elevated with a left shift
• Renal function is initially unchanged, but blood urea nitrogen and creatinine rise progressively
• Hepatic transaminases may be markedly elevated due to liver hypoperfusion. The lactic acid
level is elevated
• ABG:-hypoxemia and anion gap metabolic acidosis, which may be compensated by
respiratory alkalosis
• Cardiac markers, creatine phosphokinase and its MB fraction, and troponins I and T are
markedly elevated.

55. 55
2.Electrocardiogram:- In CS due to acute MI with LV failure, Q waves and/or >2-mm ST
elevation in multiple leads or left bundle branch block are usually present. More than one-half
of all infarcts associated with shock are anterior
3.Chest roentgenogram :-Pulmonary vascular congestion and often pulmonary edema, but
these findings may be absent in one-third of patients
• The heart size is usually normal when CS results from a first MI but is enlarged when it
occurs in a patient with a previous MI
4.Echocardiogram:- Doppler mapping demonstrates a left-to-right shunt in patients with VSR
and the severity of MR
• Proximal aortic dissection with aortic regurgitation or tamponade may be visualized, or
evidence for pulmonary embolism may be obtained

56. 56
Fig 326-2 harrison,pg no. 1761

57. 57
3. OBSTRUCTIVE SHOCK
• Obstructive shock is due to a decrease in venous return or cardiac compliance due to an
increased left ventricular outflow obstruction or marked preload decrease
• Cardiac tamponade and tension pneumothorax are common causes
• Several hemodynamic patterns may be observed, depending on the cause, from decrease
in filling pressures (as in mediastinal compressions of great veins); to trends towards
equalization of pressures in the case of cardiac tamponade; or to markedly increased
right ventricular filling pressures with low PCWP in the case of pulmonary embolism.
Cardiac output is usually decreased with increased SVR.

58. 58
CAUSES:-

59. 59
• The diagnosis of obstructive shock is based on clinical findings, the chest
radiograph, and an echocardiogram
• Pericardial tamponade:-confirmed by echocardiography, and treatment consists
of immediate pericardiocentesis or the creation of an open subxiphoid pericardial
window
• Tension pneumothorax:-Chest decompression must be carried out immediately
and, ideally, should occur based on clinical findings rather than awaiting a chest
radiograph. Release of air and restoration of normal cardiovascular dynamics are
both diagnostic and therapeutic
MANAGEMENT:-

60. 60
4. DISTRIBUTIVE SHOCK
• This type of shock is associated with not only poor vascular tone in the peripheral
circulation but maldistribution of blood flow to organs within the body also
• The CO varies, but is usually raised
• Haemodynamic profile :-
 low or normal PCWP
 high CO
 low arterial blood pressure
 low SVR.

61. 61
CAUSES:-

62. 62
SEPTIC SHOCK…..

63. 63
NEW DEFINATIONS*:-
*Singer M, Deutschman CS, Seymour CW, et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016;315(8):801-810. doi:10.1001/jama.2016.0287
**qSOFA:- Quick sequential organ failure assessment
• Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host
response to infection
• Patients with suspected infection who are likely to have a prolonged ICU stay or to die in
the hospital can be promptly identified at the bedside with qSOFA**, i.e, alteration in
mental status, systolic blood pressure ≥100 mm Hg, or respiratory rate ≥22/min
• Organ dysfunction can be identified as an acute change in total SOFA score ≥2 points
consequent to the infection. The baseline SOFA score can be assumed to be zero in
patients not known to have preexisting organ dysfunction.
• A SOFA score ≥2 reflects an overall mortality risk of approximately 10% in a general
hospital population with suspected infection.

64. 64
• Septic shock is defined as a subset of sepsis in which underlying circulatory and cellular
metabolism abnormalities are profound enough to substantially increase mortality
• Patients with septic shock can be identified with a clinical construct of sepsis with
persisting hypotension requiring vasopressors to maintain MAP ≥65 mm Hg and having a
serum lactate level >2 mmol/L (18mg/dL) despite adequate volume resuscitation.
Terms like septicemia / severe sepsis / SIRS has been REMOVED
*Singer M, Deutschman CS, Seymour CW, et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016;315(8):801-810. doi:10.1001/jama.2016.0287

65. 65
CAUSES:-
1.Peritonitis caused by spread of infection from the uterus and fallopian tubes, sometimes
resulting from instrumental abortion performed under unsterile conditions.
2.Peritonitis resulting from rupture of the gastrointestinal system, sometimes caused by
intestinal disease and sometimes by wounds.
3.Generalized bodily infection resulting from spread of a skin infection such as
streptococcal or staphylococcal infection.
4.Generalized gangrenous infection resulting specifically from gas gangrene bacilli,
spreading first through peripheral tissues and finally by way of the blood to the internal
organs, especially the liver.
5.Infection spreading into the blood from the kidney or urinary tract, often caused by colon
bacilli.

66. 66

67. 67
CLINICAL MANIFESTATIONS :-
• The manifestations of the septic response are superimposed on the symptoms and signs
of the patient’s underlying illness and primary infection
• Some patients with sepsis are normo- or hypothermic; the absence of fever is most
common in neonates, in elderly patients, and in persons with uremia or alcoholism
• Hyperventilation, producing respiratory alkalosis, is often an early sign of the septic
response
• Disorientation, confusion, and other manifestations of encephalopathy may also develop
early, particularly in the elderly and in individuals with preexisting neurologic
impairment

68. 68
• Hypotension and DIC predispose to acrocyanosis and ischemic necrosis of peripheral
tissues, most commonly the digits
• Cellulitis, pustules, bullae, or hemorrhagic lesions may develop when hematogenous
bacteria or fungi seed the skin or underlying soft tissue
• Gastrointestinal manifestations such as nausea, vomiting, diarrhea, and ileus may suggest
acute gastroenteritis. Stress ulceration can lead to upper gastrointestinal bleeding.
Cholestatic jaundice, with elevated levels of serum bilirubin (mostly conjugated) and
alkaline phosphatase, may precede other signs of sepsis

69. 69
DIAGNOSIS:-
• There is no specific diagnostic test for sepsis
• Definitive etiologic diagnosis requires identification of the causative
microorganism from blood or a local site of infection
 At least two blood samples should be obtained (from two different
venipuncture sites) for culture; in a patient with an indwelling
catheter, one sample should be collected from each lumen of the
catheter and another via venipuncture

70. 70
MANAGEMENT……

71. 71

72. 72
2016 Surviving sepsis Campaign Guidelines:-
A. INITIAL RESUSCITATION AND INFECTIOUS ISSUES
B. HEMODYNAMIC SUPPORT AND ADJUNCTIVE
THERAPY
C. OTHER SUPPORTIVE THERAPY OF SEVERE SEPSIS

73. 73
A. INITIAL RESUSCITATION AND INFECTIOUS ISSUES
• Sepsis and septic shock are medical emergencies, and we recommend that treatment and
resuscitation begin immediately
• In the initial resuscitation from sepsis- induced hypoperfusion, at least 30 mL/kg of
intravenous crystalloid fluid be given within the first 3 hours
• Following initial fluid resuscitation, additional fluids be guided by frequent reassessment of
hemodynamic status
• A target mean arterial pressure of 65 mmHg in patients with septic shock requiring
vasopressors
• Targeting resuscitation to normalize lactate in patients with elevated lactate levels as a
marker of tissue hypoperfusion

74. 74
• A fluid challenge technique be applied where fluid administration is continued as long as
hemodynamic factors continue to improve
• Crystalloids as the fluid of choice for initial resuscitation and subsequent intravascular
volume replacement in patients with sepsis and septic shock

75. 75
ANTIMICROBIAL THERAPY
• Appropriate routine microbiologic cultures (including blood) be obtained before starting
antimicrobial therapy in patients with suspected sepsis and septic shock if it results in no
substantial delay in the start of antimicrobials (i.e, <45 minutes)
• Administration of intravenous antimicrobials be initiated as soon as possible after
recognition and within 1hour for both a) septic shock and b) sepsis without shock
• Empiric broad-spectrum therapy with one or more antimicrobials for patients presenting
with sepsis or septic shock to cover all likely pathogens (including bacterial and potentially
fungal or viral coverage)
• If combination therapy is used for septic shock, de-escalation is recommended, with
discontinuation of combination therapy within the first few days in response to clinical
improvement and/or evidence of infection resolution. This applies to both targeted (for
culture-positive infections) and empirical (for culture-negative infections) combination
therapy

76. 76
• Antimicrobial treatment duration of 7‒10 days is adequate for most serious infections
• Daily assessment for de-escalation of antimicrobial therapy in patients with sepsis
• Measurement of procalcitonin levels can be used to shorten the duration of
antimicrobial therapy in sepsis patients
• Prompt removal of intravascular access devices that are a possible source of sepsis or
septic shock after other vascular access has been established

77. 77
B. HEMODYNAMIC SUPPORT AND OTHER ADJUNCTIVE THERAPY
• If hypotension persists after the initial volume resuscitation, infusion of a vasoconstrictor drug
(vasopressor) like norepinephrine or dopamine should begin. Vasoconstrictor drugs must be
infused through a central venous catheter, and the goal is to achieve a mean arterial pressure
(MAP) ≥ 65 mm Hg
• Norepinephrine as the first-choice vasopressor. For norepinephrine, start with a dose rate of
0.1 μg/kg/min and titrate upward as needed. Dose rates up to 3.3 μg/kg/min are successful in
raising the blood pressure in a majority of patients with septic shock
• If the desired MAP is not achieved at a dose rate of 3 – 3.5 μg/kg/min, add dopamine as a
second vasopressor
VASOPRESSOR THERAPY:-

78. 78
• For dopamine, start at a dose rate of 5 μg/kg/min and titrate up- ward as
needed. Vasoconstriction is the predominant effect at dose rates above 10
μg/kg/min
• .If the desired MAP is not achieved with a dose rate of 20 μg/kg/min,
hypotension is refractory to norepinephrine and dopamine, vasopressin
may be effective in raising the blood pressure. (Vasopressin is used as an
additional pressor rather than a replacement for norepinephrine or
dopamine.) The dose range for vasopressin is 0.01–0.04 units/min, but in
septic shock is 0.03 units/min

79. 79
Role of Corticosteroids:-
• Do not use intravenous hydrocortisone to treat septic shock patients if adequate fluid
resuscitation and vasopressor therapy are able to restore hemodynamic stability. If this is
not achievable, then intravenous hydrocortisone alone at a dose of 200 mg per day
• When low-dose hydrocortisone is given, then use continuous infusion rather than
repetitive bolus injections
• Corticosteroids should not be administered for the treatment of sepsis in the absence of
shock

80. 80
C. OTHER SUPPORTIVE THERAPY OF SEVERE SEPSIS
Administration of Blood products:-
• Red blood cell transfusion occur only when hemoglobin concentration decreases to
<7.0‒7.5 g/dL in adults in the absence of extenuating circumstances, such as myocardial
ischemia, severe hypoxemia, or acute hemorrhage
• Prophylactic platelet transfusion when counts are <10,000/mm3 (10 x 109/L) in the
absence of apparent bleeding and when counts are <20,000/mm3 (20 x 109/L) if the
patient has a significant risk of bleeding. Higher platelet counts (≥50,000/mm3 [50 x
109/L]) are advised for active bleeding, surgery, or invasive procedures

81. 81
Mechanical ventilation and weaning
• Target a tidal volume of 6 mL/kg predicted body weight in patients with sepsis-induced
ARDS vs 12 mL/kg
• Upper limit goal for plateau pressures of 30 cmH20 over higher plateau pressures in adult
patients with sepsis-induced severe ARDS
• Higher positive end expiratory pressure (PEEP) over lower PEEP in adult patients with
sepsis-induced moderate to severe ARDS
• Using prone over supine position in adult patients with sepsis-induced ARDS and a
PaO2/FiO2 ratio <150
• Use of HFOV in adult patients with sepsis-induced ARDS

82. 82
• Mechanically ventilated sepsis patients be maintained with the head of the bed elevated
between 30 and 45 degrees to limit aspiration risk and to prevent the development of VAP
• Continuous or intermittent sedation be minimized in mechanically ventilated sepsis
patients, targeting specific titration endpoints
• Use of spontaneous breathing trials in mechanically ventilated sepsis patients with sepsis
when they satisfy the following criteria: a) arousable; b) hemodynamically stable (without
vasopressor agents); c) low ventilatory and end-expiratory pressure requirements; and d)
low FiO2 requirements which can be safely delivered with a face mask or nasal cannula.
If the spontaneous breathing trial is successful, extubation should be considered

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GLUCOSE
• Commence insulin dose when two consecutive blood glucose
levels are >180 mg/dL
• Blood glucose values be monitored every 1 to 2 hours until
glucose values and insulin infusion rates are stable, then every 4
hours thereafter in patients receiving insulin infusions

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VTE Prophylaxis
• Pharmacologic prophylaxis (unfractionated heparin [UFH] or low
molecular weight heparin [LMWH]) against VTE in the absence
of contraindications to the use of these agents
• Mechanical VTE prophylaxis when pharmacologic VTE is
contraindicated

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Stress Ulcer prophylaxis
• Stress ulcer prophylaxis be given to patients with sepsis or
septic shock who have risk factors for GI bleeding
• Either proton pump inhibitors (PPIs) or histamine-2 receptor
antagonists (H2RAs) when stress ulcer prophylaxis is indicated

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NUTRITION
• Administration of early full enteral nutrition rather than early parenteral
nutrition alone or parenteral nutrition in combination with enteral
feedings in critically ill patients with sepsis or septic shock who can be
fed enterally
• Use of prokinetic agents in critically ill patients with sepsis or septic
shock and feeding intolerance

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ANAPHYLACTIC SHOCK….

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• Anaphylaxis is an acute multiorgan dysfunction syndrome produced by the
immunogenic release of inflammatory mediators from basophils and mast cells
• The characteristic feature is an exaggerated immunoglobulin E (IgE) response to an
external antigen; i.e., a hypersensitivity reaction type I
• The manifestations of anaphylaxis typically involve the skin, lungs, gastrointestinal
tract, and cardiovascular system
• Identical manifestations can occur without the involvement of IgE; these are called
anaphylactoid reactions, and are not immunogenic in origin
• Common triggers for anaphylactic reactions include food, antimicrobial agents, and
insect bites, while common triggers for anaphylactoid reactions include opiates and
radiocontrast dyes

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• Anaphylactic shock is an immediate threat to life, with profound
hypotension from systemic vasodilatation and massive fluid loss through
leaky capillaries.
• The hemodynamic alterations in anaphylactic shock are similar to those in
septic shock, but are often more pronounced

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PATHOPHYSIOLOGY

91. 91

92. 92
TREATMENT

93. 93
 Volume Resuscitation
• Aggressive volume resuscitation is essential in anaphylactic shock because at least
35% of the intravascular volume can be lost through leaky capillaries , which is
enough to produce hypovolemic shock Volume resuscitation can begin by infusing 1–
2 liters of crystalloid fluid (or 20 mL/kg), or 500 mL of isooncotic colloid fluid (e.g.,
5% albumin), over the first 5 minutes . Thereafter, the infusion rate of fluids should
be tailored to the clinical condition of the patient
 Refractory Hypotension
• Persistent hypotension despite epinephrine infusion and volume resuscitation can be
managed by adding glucagon or another vasopressor such as norepinephrine or
dopamine

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95. 95
NEUROGENIC SHOCK
• Neurogenic shock is a devastating consequence of spinal cord injury (SCI),
also known as vasogenic shock. Injury to the spinal cord results in sudden
loss of sympathetic tone, which leads to the autonomic instability that is
manifested in hypotension, bradyarrhythmia, and temperature dysregulation
• Neurogenic shock is most commonly a consequence of traumatic spinal
cord injuries, more in cervical spine injuries
• Other causes include inadvertent cephalad migration of spinal anesthesia, or
devastating head injury, Guillain-Barre syndrome, transverse myelitis

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DIAGNOSIS
• Neurogenic shock is most commonly associated with a blunt cervical spine injury
• Neurogenic shock should be considered only after a hemorrhagic shock has been ruled
out in a traumatic patient, the presence of vertebral fracture or dislocation raises the
concern for neurogenic shock
• Bradyarrhythmia, hypotension, flushed warm skin are the classic signs associated with
neurogenic shock
• The joint committee of the American Spinal Injury Association and the International
Spinal Cord Society propose the definition of neurogenic shock to be autonomic nervous
system dysfunction that includes symptoms such as orthostatic hypotension, autonomic
dysreflexia, temperature dysregulation. A focal neurologic deficit is not necessary for the
diagnosis of neurogenic shock

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TREATMENT
• Initial management of neurogenic shock is focused on hemodynamic stabilization.
Hypotension should be treated first to prevent secondary injury. The first-line treatment for
hypotension is intravenous fluid resuscitation
• If hypotension persists despite euvolemia, vasopressors and inotropes are the second lines
• Phenylephrine is commonly used as it is a pure alpha-1 agonist that causes peripheral
vasoconstriction to counteract the loss sympathetic tone
• Epinephrine ,for refractory cases of hypotension
• Keep the mean arterial pressure (MAP) at 85–90 mmHg for the first 7 days to improve
spinal cord perfusion
• Initial spine immobilization is important to prevent further spinal cord injury

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1.Guyton & Hall: Textbook of Medical Physiology, 12th ed
2.Robbin’s Basic pathology, 9th ed
3.Harrison’s principle of internal medicine, 19th ed
4.Miller’s Anesthesia, 8th ed
5.Wylie and Churchill-Davidson's A Practice of Anesthesia , 5th ed
6.Marino’s The ICU Book, 4th ed
7.Tintinalli’s Emergency Medicine ,A Comprehensive Study Guide ,8th ed
8.SHOCK – A SHORT REVIEW ,IJA 2003,Dr. A. K. Sethi, Dr. Prakash Sharma, Dr. Medha Mohta, Dr. Asha Tyagi
9.Cardiogenic Shock,Harmony R. Reynolds and Judith S. Hochman,Circulation. 2008;117:686-697, February 4, 2008
https://doi.org/10.1161/CIRCULATIONAHA.106.613596
10.Baskett PJ. ABC of major trauma. Management of hypovolaemic shock. BMJ: British Medical Journal. 1990 Jun
2;300(6737):1453
11.Singer M, Deutschman CS, Seymour CW, Shankar-Hari M, Annane D, Bauer M, Bellomo R, Bernard GR, Chiche JD,
Coopersmith CM, Hotchkiss RS. The third international consensus definitions for sepsis and septic shock (sepsis-3). Jama.
2016 Feb 23;315(8):801-10
12.Rhodes A, Evans LE, Alhazzani W, Levy MM, Antonelli M, Ferrer R, Kumar A, Sevransky JE, Sprung CL, Nunnally ME,
Rochwerg B. Surviving sepsis campaign: international guidelines for management of sepsis and septic shock: 2016. Intensive
care medicine. 2017 Mar 1;43(3):304-77
13.Dave S, Cho JJ. Shock, Neurogenic. StatPearls ,www.ncbi.nlm.nih.gov/books/NBK459361
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