SHOC

K PATHOPHYSIOL
OGY CLINICAL
FEATURES
DR ANKIT MANAGEMENT
SHARMA
DR ARUN KUMAR
M
1
SAMUEL V GROSS,
1872 “Shock is the
manifestation of
the rude unhinging
of the machinery
of life”

2
 HISTORIC
AL
PERSPECTI
• Ambroise Paré (1510) – Fluids to injured patients
• ‘Shock’ – 1743 – act of impact/ collision
VE
• Guthrie (1815) – described physiological instability
• Crile (1899) – Importance of measuring BP
• Claude Bernard – Milieu intérieur
• Walter B. Cannon – Homeostasis
• WW I – Disturbance of nervous system
• Alfred Blalock (1934) – 4 categories of shock
• Carl John Wiggers (1950) – Wiggers prep

3
Definitio
n cellular respiration
A systemic state of tissue hypo-perfusion, which is inadequate for
normal

 Systemic – global phenomenon

 Hypoperfusion (relative/ absolute)
 Inadequate cellular respiration
 Anaerobic, dysfunction
 Body responses thereof

4
 Type
•sHypovolemic
• Cardiogenic
• Septic (vasogenic)
• Neurogenic
• Traumatic
• Obstructive

5
 Hypovolemic
• Hemorrhagic
shock
• Trauma
• Bleeding disorders
• GI/ GU bleed
• Non- hemorrhagic
• Dehydration
• “Inter compartmental fluid mal-adjustments”
• Third spacing

6
Cardiogenic Shock
• Pump failure

• Adequate but ineffective intravascular

volume.
• Cardiac causes
• Pulmonary embolism

• High mortality rates

8
 Cardiogenic
•shock
Hemodynamic criteria:
1.Sustained Hypotension (i.e. SBP <90 mm Hg
for at least 30 minutes)
2.Reduced Cardiac Index (<2.2 L/min per
square meter) &
3.Elevated Pulmonary Artery Wedge Pressure
(>15 mm Hg)

9
SEPTIC SHOCK
• Four sepsis-related clinical syndromes = Four steps of
increasingly exaggerated systemic inflammatory responses

 SIRS
 Sepsis
 Severe Sepsis (Sepsis Syndrome)
 Septic Shock

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DEFINITIONS DESCRIBING
THE CONDITION OF
SEPTIC PATIENTS
Bacteremia: Bacteria in blood
Positive blood cultures

Septicemia: Microbes or their toxins in blood

12
DEFINITIONS DESCRIBING
THE CONDITION OF
SEPTIC
SIRS: PATIENTS
Two or more of the following

(1) Temperature >38°C or <36°C
 (2) Heart Rate > 90/ min
 (3) Respi rate > 24/ min
 (4) TLC >12,000/mm3 or
<4,000/mm3)
or >10% bands on PBS
◦SIRS may have a noninfectious etiology
Sepsis: SIRS that has a proven/ suspected microbial etiology
13
DEFINITIONS DESCRIBING
THE CONDITION OF
SEPTIC
Severe PATIENTS
Sepsis (Similar
organ dysfunction:
to sepsis syndr): Sepsis with one or more signs of

1. Cardiovascular
2. Renal
3. Respiratory
4. Hematologic
5. Unexplained metabolic acidosis
6. Adequate fluid resuscitation
14
DEFINITIONS DESCRIBING
THE CONDITION OF
SEPTIC PATIENTS
Septic Shock: Sepsis + Hypotension
or
Need for vasopressors to
maintain systolic BP 90 mmHg
or MAP70 mmHg

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DEFINITIONS DESCRIBING
THE CONDITION OF
SEPTIC PATIENTS
Refractory septic shock: Septic shock
◦lasting for >1 h
◦Not responding to fluid or pressor administration

MODS: Dysfunction of more than one organ system,

requiring intervention (individual organ support) to maintain
homeostasis

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 NEUROGENIC
•SHOCK
Acute loss of sympathetic vascular tone
• Loss of vascular resistance
◦Pooling in capacitance vessels
◦Reduced preload
◦Poor cardiac output
◦Inadequate pressure in arterial system
to maintain capillary perfusion

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NEUROGENIC SHOCK
Etiology:
◦High cervical spinal cord injury (vertebral body #)
◦inadvertent cephalad migration of spinal
anaesthesia
◦epidural hematoma or devastating head injury
Failure of fluid resuscitation to improve hemodynamics, where no source of blood
loss or sepsis can be identified
Vasopressors are necessary to treat this condition

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TRAUMATIC SHOCK
•Hemorrhage overtly controlled, but
patients continues to lose plasma volume
into the interstitium
• Secondary microcirculatory injury
• Excessive pro-inflammatory response
• Third spacing
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 OBSTRUCTIVE
•SHOCK
Reduction in preload due to mechanical
obstruction of cardiac filling

•Common causes: cardiac tamponade,

tension pneumothorax, massive pulmonary
embolus or air embolus

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 PATHOPHYSIOLOGY OF
SHOCK
• Initial response driven by
• Tissue hypoperfusion
• Developing cellular energy deficit.
• Demand-supply mismatch
• Neuro-endocrine & inflammatory response (proportional
to degree & duration of shock)
• The specific responses depends on etiology of shock

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SHOCK INDUCED VICIOUS CYCLE 22
 CELLULAR
PATHOPHYSIOLOGY
• Compensation/ Dysfunction/ Death

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 ↓ O2 concn in cells
↓
↓ oxidative phosphorylation
↓
↓ ATP synthesis
↓
shift from aerobic to anaerobic glycolysis
↓
Pyruvate converted to lactate
↓
accumulation of lactate & inorganic phosphate, thus ↓ pH
↓
intracellular metabolic acidosis  lactate & other wastes exit cells
↓
systemic metabolic acidosis

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 MICROVASCUL
AR
•PATHOPHYSIOL
α1 receptors – vasoconstriction
•OGY
ẞ2 receptors - vasodilation.
•Shock  norepinephrine & epinephrine from
adrenal medulla → α1 receptors
•Other constrictors: A-II, vasopressin, endothelin 1,
and TxA2
• Vasodilators: PG I2, NO and adenosine

28
 Hypoxia & acidosis
↓
Complement & neutrophil activation
↓
Free radical & cytokine release
↓
Injury to capillary endothelial cells
↓
Further activation of immune & coagulation systems
↓
Damage to endothelium with loss of integrity
↓
Leaky capillary endothelium
↓
Tissue edema & cellular hypoxia

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CARDIOVASCUL
AR
PATHOPHYSIOL Shock

OGY ↓
↓ Preload & ↓ Afterload
↓
↑ sympathetic output
↓
catecholamine release from adrenal medulla
↓
↑ heart rate & contractility
venous and arterial vasoconstriction (Except in sepsis)

30
 CARDIOVASCUL
AR
•PATHOPHYSIOL
Arterial vasoconstriction with regional
OGY
variations
•Shunting of blood away from less essential
organ beds such as the intestine, kidney, and
skin
• Brain & heart – autoregulatory
mechanisms
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 PULMONARY
•PATHOPHYSIOLOGY
Tachypnea
• ↑ minute ventilation & ↑ CO2 excretion
• Compensatory respiratory alkalosis
• Resuscitation induced O2 free radical injury
• ALI & ARDS
• Non cardiogenic pulmonary edema

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 RENAL
PATHOPHYSIOLOGY
• Decreased renal blood flow
• RAS activation
• ↓ GFR + ↑ aldosterone & vasopressin → Oliguria

• Further vasoconstriction → ↑ sodium & water

retention → edema
• Toxic tubular injury & Tubular obstruction

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 ENDOCRINE
•PATHOPHYSIOLOGY
Na+ & water retention  K+ & H+ lost
• Hypovolaemia  ADH
• Adrenergic drive  Norepinephrine release
• Vasoconstriction
• ↑ glycogenolysis & ↑ gluconeogenesis
• ↓ Insulin release

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ENDOCRINE CRH (Hypothalamus)

PATHOPHYSIOLOGY ↓
ACTH (pituitary)
↓
Cortisol (Adrenal Cortex)
↓
Cortisol + Epinephrine + Glucagon  Catabolic state
↓
Gluconeogenesis & Insulin resistance
↓
Hyperglycemia, Muscle protein break down, lipolysis

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 METABOLIC
DERANGEME
•NTS
Disruption of C-P-L metabolism
• Anaerobic metabolism  Lactate
• ↑ Hepatic gluconeogenesis
• Hepatic lipogenesis  ↑ TG
• Protein catabolism → muscle wasting

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INFLAMMATORY
& IMMUNE
RESPONSE
Pro-inflammatory Anti-inflammatory
IL-1α/ẞ IL-4
IL-2 IL-10
IL-6 IL-13
IL-8 IL-1Ra
IFN-ϒ PGE2
TNF-α TGF-β
PAF
TNFR- I/II

37
 INFLAMMATORY
& IMMUNE
•RESPONSE
MODS
• Counter-regulatory immune response
• Delayed MOF

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 SEPTIC
SHOCK
• Culture proven etiology +/-
• Any class of micro-organism
•Gram (-) ve bacteria > Gram (+) ve bacteria >
polymicrobial infection > fungi
•Gm (-) ve bacteria = Enterobacteriaceae, pseudomonads,
Haemophilus etc.
•Gm (+) ve bacteria = S.aureus, coagulase (-) ve staph,
enterococci, S.pneumoniae etc.

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SEPTIC SHOCK
Myocardial depression
+ Hypovolemia
+ other factors
↓
Tissue hypoxia (hypodynamic pd)
↓
↑ blood lactate & ↓ central venous O2 saturation

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SEPTIC SHOCK
After fluid administration
↓
↓ peripheral vascular resistance
(vasodilatory phase)
Hallmark of septic shock

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Clinical Features &
Management

45
Severity of shock
Compensated shock

Decompensation
• Mild shock
• Moderate shock
• Severe shock

Unresuscitable Shock

MOF

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 Severity of
shock
Compensated shock

◦Loss of up to 15% of circulatory volume

◦ Maintain central blood volume

◦ If prolonged (>12 hrs)  Ischaemia-Reperfusion effect

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 Severity of shock
Decompensation

◦Loss of > 15% of circulating volume.

◦ Progressive Renal, Respiratory & Cardiovascular decompensation.

◦ Hypotension  >30-40% volume loss.

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Severity of shock

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Hemorrhagic
shock

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Hemorrhagic shock
 Most common cause of shock in the surgical or trauma patients

 Young patients vs elderly patients

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Hemorrhagic
shock
Classification of hemorrhage

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Hemorrhagic shock
 Approach to Hemorrhagic shock
 Identify haemorrhage

 Immediate resuscitative maneuvers

 Identify the site of haemorrhage

 Haemorrhage control

 Damage control resuscitation

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 Hemorrhagic shock
 Treatment concurrently with diagnostic evaluation

 Time dependent survival

 Resuscitative maneuvers

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Hemorrhagic shock
 History
 Root cause of hemorrhage & its site

 Any underlying Pathology

 Any co-morbidities/medications

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 Hemorrhagic
shock
 Symptoms & Signs:
 Agitation, Cold clammy extremities
 Tachycardia, Hypotension
 Pallor
 Weak or absent peripheral pulses
 Prolonged capillary refill time
 Systemic examination
 Symptoms specific to site of Hemorrhage
56
Hemorrhagic
shock
 Site specific Symptoms & Signs:

 Penetrating wounds / Blunt trauma

 Sites that can harbor sufficient

extra-vascular volume:
 Intrathoracic (2-3L/ pleural cavity)
 Intraabdominal
 Retroperitoneal
 # long bones 57
 Hemorrhagic
shock
 Investigations
 Hematological & Biochemical Investigations

 Lactate levels

 Blood grouping & cross matching

 Radiological investigations as indicated

58
 Hemorrhagic
shockhypotension
 Damage control resuscitation
 Permissive

 Use of limited crystalloids and blood products

 Anticipate and treat coagulopathy

 Hypothermia

 DCS
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 Hemorrhagic shock
 Fluid therapy

 Crystalloid

 Hypotonic solutions

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 Hemorrhagic shock
 Fluid therapy : Dynamic Fluid Response
 To determine shock status

 250-500ml bolus over 5-10min

 HR, BP & CVP are measured

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 Hemorrhagic
shock
Responders
• Sustained improvement in CVS status after bolus
• No active bleeding, require fluids to attain normal volume status

Transient Responders
• Initial improvement followed by reverting to previous state over 10-20 min
• Moderate ongoing fluid losses

Non responders
• No improvement in CVS status following bolus
• Severely volume depleted and likely to have ongoing loss( persistent uncontrolled
Hemorrhage)
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 Hemorrhagic
shock
 Transfusion of blood and blood products
Blood product Aim
PRBC Hb 7-9 gm/dl
Platelets > 50,000/ml

 Coagulation factor-based products

63
 Hemorrhagic
shock
Monitoring of response
◦Clinical : Conscious level, BP, Urine output
◦ECG
◦Pulse oximetry
◦CVP, Invasive BP monitoring
◦Cardiac output
◦Base deficit & serum lactate

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Hemorrhagic
shock

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 Traumatic
shock
 Initial resuscitation

 Control of Hemorrhage

 Early stabilization of the fractures, debridement or evacuation of

hematoma

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Septic
Shock

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Septic
shock

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 SEPSIS SIX
The Sepsis Six is the name given to a bundle of medical therapies designed to reduce
the mortality of patients with sepsis.
The Sepsis Six consists of three diagnostic and three therapeutic steps – all to be
delivered within one hour of the initial diagnosis of sepsis.
◦Deliver high-flow oxygen.
◦Take blood cultures.
◦Administer empiric intravenous antibiotics.
◦Measure serum lactate and send full blood count.
◦Start intravenous fluid resuscitation.
◦Commence accurate urine output measurement.

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Management of severe sepsis
 Initial Resuscitation and Infection Issues

 Hemodynamic Support and Adjunctive Therapy

 Supportive Therapy of Severe Sepsis

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Initial Resuscitation and Infection
Issues
A. Initial Resuscitation
B. Screening for Sepsis and Performance Improvement
C. Diagnosis
D. Antimicrobial Therapy
E. Source Control
F. Infection Prevention

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 A. Initial Resuscitation
Resuscitation of patients with sepsis- induced tissue
hypoperfusion
◦defined as hypotension persisting after initial fluid challenge or blood
lactate concentration ≥ 4 mmol/L

EGDT (first 6 hrs of resuscitation)

◦a) CVP 8–12 mm Hg
◦b) MAP ≥ 65 mm Hg
◦c) Urine output ≥ 0.5 mL/kg/hr
◦d) Scvo2 or Svo2 70% or 65%, respectively

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B. Screening for Sepsis and
Performance Improvement
 Routine screening of seriously ill patients for severe sepsis to
 increase the early identification of sepsis
 allow implementation of early sepsis therapy

Performance improvement efforts to improve patient outcomes

and decrease sepsis-related mortality.

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74
 C. Diagnosis
 Cultures
 Imaging studies
 1,3 β-d-glucan assay ,mannan and anti-mannan antibody assays

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D. Antimicrobial
Therapy
 Initial empiric anti-infective therapy
 Broad spectrum
 Anti fungals
 Reassessed daily for potential de-escalation
 Combination empiric therapy
 Duration & De-escalation

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 E. Source
Control
 Intervention for source control within the first 12 hr of diagnosis.

77
Haemodynamic support & Adjunctive
therapy
 Fluid therapy
 Vasopressors
 Inotropic support
 Corticosteroids

78
Haemodynamic support & Adjunctive
therapy
 Fluid therapy  Ionotropic agents : Dobutamine
 Crystalloids
 Albumin
 Corticosteroid
 Vasopressor
s
 Noradrenaline
 Adrenaline
 Vasopressin
 Dopamine
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 Supportive therapy
 Blood products administration  Renal replacement therapy
Mechanical ventilation of sepsis  DVT prophylaxis

induced ARDS  Stress ulcer prophylaxis

Sedation, analgesia & neuromuscular  Nutrition

blockade  Setting goals of care

 Glucose control

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Cardiogenic
Shock

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Cardiogenic
shock
Causes:
◦ Acute MI (most common)
◦ Arrythmia
◦ End stage cardiomyopathy
◦ Myocarditis
◦ Severe myocardial contusion
◦ LV outflow obstruction
◦ Obstruction to LV filling
◦ MR
◦ Acute aortic insufficiency
◦ Metabolic
◦ Drug reactions
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 Cardiogenic
shock
Diagnosis

 ECG & ECHO

 CXR

 ABG

 Cardiac enzymes

 Invasive monitoring

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Cardiogenic
shock
 Treatment
 Aims of treatment
 Adequate oxygenation

 Judicious fluid administration

 Adequate Analgesia

 Correcting electrolyte imbalances

84
Cardiogenic
shock
 Treatment

 Ionotropic support (Dopamine/Dobutamine)

 Treatment of cause

85
Obstructive
Shock

86
Obstructive
shock
Causes:
◦ Tension Pneumothorax
◦ Pericardial Tamponade
◦ Pulmonary embolus
◦ IVC obstruction [Gravid uterus, DVT, Neoplasm]
◦ Increased Intra-thoracic pressure [ Excess end-expiratory pressure, Neoplasm]

87
 Obstructive
shock
Diagnosis
 Diagnosis is clinical

 Chest X-Ray

 Echocardiography

 Pericardiocentesis

 Treatment of the cause

88
Neurogenic
Shock

89
 Neurogenic
shock
Causes
 Spinal cord Trauma

 Spinal cord Neoplasm

 Spinal / Epidural anesthesia

90
Neurogenic
shock
Diagnosis:
 Hypotension with bradycardia

 Warm extremities

 Motor and sensory deficits

 Radiographic evidence of vertebral fracture

91
 Neurogenic
shock
Treatment
 Fluid resuscitation

 Ionotropic support

 Operative attempt to stabilise the vertebral fracture.

92
THANK YOU

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