Mastering Shock Management: Causes, Classification, & Stages

When there is a sudden drop in blood flow throughout the body, it leads to shock. It is a critical condition that might result from trauma, heatstroke, blood loss, allergic reaction, severe infection, poisoning or other causes.

At the time when a person goes into shock, the organs don’t get enough blood or oxygen and if shock is left untreated, it can lead to permanent organ damage or in the worst cases, even death. 

Learn more about this critical condition and scale up your NEET SS Medicine preparation. 

Let’s begin.

• Decrease oxygen delivery to the tissues generalized circulatory failure & / or
• Decrease uptake of oxygen by the tissues. E.g. Septic shock 

Pathophysiology of shock

• Anaerobic metabolism of glucose 
• Glucose → pyruvate → lactate → causes acidosis → cellular swelling & cell death

Stages Of Shock

Stage I 

• Pre shock: compensated shock
• When a state of circulatory failure there will be several compensatory mechanism gets activated to revert the shock 
  ↓
• No evidence- Hypotension and no obvious damage ↑lactate levels 
• Best stage to correct the shock 

Stage II 

• Decompensated shock
• Compensatory mechanism gets failed
• Shock become evident
  ↓
• Hypotension & organ damage (map <60 m Hg) 

Stage III 

• Irreversible shock 
• Reversible organ injury 

Classification Of Shock

• Shubin and weil classification
• Hemodynamic profiling helps in making decision for treatment 
  • Hypovolemic shock: ↓ cardiac output decrease venous return 
  • Cardiogenic shock 
    • Causes MI, Arrhythmias 
  • Obstructive shock 
    • Cause: Cardiac tamponade 
    • Restrictive cardiomyopathy 
    • Massive pulmonary embolism 
  • Septic shock: Most common cause of shock
    • Distributive shock
      • ↓ Systemic vascular resistance 
      • Peripheral Vasodilation

Important Causes Of Shock

Classification of Hemorrhagic shock Hypertension occurs in class III & IV 

Evaluation & Approach To Shock

• Early recognition
  • Shock index heart rate systolic blood pressure: HR/ SBP 
• Normal 0.5 - 0.7
• 70.9 need for transfusion 
• Post intubation hypotension 

• Serum lactate measurement
  • Done serially; rises very early before hypotension
    Indicates: Tissue hypoperfusion 
• Q SOFA
  • To recognize septic shock 
• Capillary refill time
• < 2 sec : > 3 sec 

Early indication of  shock, distributive shock; normal inspiration: IVC collapse

IVCCI = Max Diameter – Min Diameter/ Max diameter x 100

• Stroke volume variation: When patient is on ventilation
• > 12% during breathing cycle
  • ↓ Fluid responsive capillary refill time is normal
• Race protocol: Rapid Assessment for cardiac echocardiogram quick assessment of LV function
  • (Passive Leg Rise) PLR-45°
  • CO or pulse pressure
  • Inferior vena cava (IVC)
  • Collapsing → fluid deficit 

Management

• Fluids: 30 ml/kg (Loading dose)
• Methods to assess the response of Rx
• Passive leg raising test 

↓

Pulse pressure ↑↑ → patient responding

• Vasopressors

• Transfusion
  • Hb cut off < 7 g ms% → Target Hb

Sepsis And Septic Shock

DEFINITION OF SEPSIS

• Life threatening organ dysfunction caused by dys-regulated host response to infection
  • Diagnostic criteria

• Definition Septic shock
  • Subset of sepsis where Cardiovascular, cellular, metabolic dearangements occurs with high rate of mortality

Incidence

• 19 million/year (world)
• INDICAPS TRIAL: 10% of ICU patients were diagnosed sepsis.
  • Etiology
• According to EPIC 2 study
• Gram positive: 47%
  • Lipo teichoic Acid
    Gram positive Bacteria
    ↓
    Recognized by

• Pattern recognition receptors
  • Toll Like receptor (TLR)
  • NOD responsible for “Inflammasome” response
  • RIG-1 receptor
  • C type lectin
• Toll like receptors
  •  4 – Lipopolysaccharide
  • 2 – Lipoteichoic acid Gram +ve
• Staphylococcus 
• Streptococcus 
• Gram Negative - 62% 
• M/c Globally
  • E.Coli 
  • Pseudomonas
  • Klebsiella 
• Fungi -19%
  • Candida albicans (m/c)
  • Non candida - Resistant to azoles, treated with ECHINOCANDINS 

Common Source Or Antecedent Infection

• Pneumonia > 50% (most common) 
• Abdominopelvic infection (UTI / Pyelonephritis) 

Pathophysiology Of Sepsis

• ↑ Pro inflammatory cytokines 
• ↑ Anti-inflammatory cytokine 
• ↑ VascuIar permeability 
• Pro-coagulant state
  • Immune response  (Innate Adaptive)
• Recognizes pathogen Associated “Microbial pattern”
  • Lipopolysaccharide – Gram negative bacteria
• Up regulation of NFK
  ↓
  ↑↑ inflammatory cytokines → Leading to organ damage

• Microbial factors (peptides): Activates factor XIII

Management: 2016 Survival Sepsis Camp Guidelines

• Early Goal directed therapy(old), not used now)
• Obtain blood culture before Antibiotics
• Administer broad spectrum Antibiotics
• Begin rapid administration of 30 ml/Kg crystalloids for hypotension or lactate > 4 mmol/L
• Apply vasopressor if hypotension during or after fluid resuscitation to achieve mean arterial pressure > 65 mmHg

Adjunctive Rx

1. Drotrecogin alpha

2. Ulinastatin – Protease inhibitor, not effective

3. Hydrocortisone

             ↓

   HYPERSS TRIAL

• Not reduce the mortality / not halts the progression to shock
• Shock
  • Fluids
  • Ionotropes 

• 200 mg/day. Divided Dose: 1-1-0 
• 100 mg 100 mg (8 AM – 4 PM)

Key SSC Guidelines 2016 Recommendations

Antibiotics 

• The risk/ benefit ratio favors rapid administration of antibiotics before the culture results
• In septic shock or sepsis each hour delay in administration of antibiotics result in increased in mortality (3-7%)
• Hydroxy Ethyl starches (HES) are not used for intravascular volume replacement in Septic shock

• 1^st choice of vasopressors: Nor Epinephrine 
• 2^nd choice of vasopressors: Vasopressin (up to 0.030/min) 
• 3^rd choice of Vasopressors : Epinephrine
• Vasopressin can be used to ↓ the dose of Norepinephrine & to achieve MAP target 
• Dopamine can be given only in patient with low risk of Tachyarrhythmia & absolute or achieve bradycardia
• Low dose of dopamine for renal protection not indicated.
• Dobutamine is used for patient who are having evidence of persistent Hypo perfusion despite adequate fluid loadings the use of Vasopressors agents
• All patient requiring vasopressor have an arterial catheter to measure the mean arterial pressure
• Pro calcitonin level can be used to support shortening the duration of anti-microbial therapy in sepsis patient \
• It also helps in discontinuation of empirical antibiotics 

Fluids

• Fluid of choice Crystalloids (Ringer lactate) 30 ml/kg 

+

            Albumin - can be used for initial resuscitation & subsequent Intravascular volume        replacement

• Corticosteroids
  • IV hydrocortisone is used for septic shock at a dose of 200 mg/day only when there is hemodynamic initially despite adequate fluid resuscitation and vasopressor therapy 
• Blood & products
  • RBC transfusion is indicated when Hemoglobin concentration decrease to 7 gm% 
  • Target Hb → 7 gm% 

• No role of FFP (Fresh frozen Plasma) to correct clotting abnormalities in the absence of bleeding or planned invasive procedures 
• Indication of platelet transfusion < 10000/mm³ in the absence of bleeding 
• Platelet count 10000 to 20000 : Platelet transfusion in indicated when there is increased risk of bleeding
• Target platelet counts 50000/ mm³ advised for active bleeding, surgery, invasive procedures 
• IV immunoglobulin is not indicated in patient with Septic shock
• Ventilator Strategies
  • Tidal volume: 6 mL/kg 
  • Plateau pressure < 30 cm/H₂O
  • High peep
  • Prone positioning 

• Sepsis induced ARDS 
• PaO₂ / FiO₂ mm < 150 

• High frequency oscillatory ventilation is not recommended in patients with sepsis induced ARDS 
• In mechanically ventilated patients. head end of the bed elevated between 30 and 45° to limit aspiration risk and to prevent the development of Ventilator associated Pneumonia

And that is everything you need to know about the treatment for shock. Hope you found this blog helpful for your NEET SS General Medicine preparation. For more informative and interesting posts like these, keep reading PrepLadder’s blogs.