Definition

• Circulation fails to meet the nutritional needs of the cells,

• Fails to remove the metabolic waste products
• Discrepancy in vascular bed and IVF
• Low blood flow state in vital organs
Types
• Hypovolaemic
• Cardiac
• Traumatic
• Distributive shock
• Nuerogenic
• Vasovagal
• psychogenic
• Septic
• Anaphylaxis
• Obstructive
 PATHOPHYSILOGY
Any Cause Of Shock Further Concentration Of Urine
↓ ↑
Low Cardiac Output ADH Is Released
↓ ↑
Vasoconstriction Salt And Water Retention
↓ ↑
Tachycardia Aldosterone Release
↓ ↑
Dynamic Circulation ↓ Further Vasoconstriction
↓ ↑
Tachypnoea Renin Angiotensin Mechanism
↓ Gets Activated
Peripheral Veins Constricts ↑
↓ GFR ,Urine Output ↓
Renal Blood Flow ↓
PATHOPHYSILOGY …
When shock persists Hypoxia
↓
↓ Anaerobic metabolism
cardiac output falls further ↓
Lactic acidosis
↓ ↓
Hypotension and tachycardia Cell wall damage
↓
↓ Sodium and calcium enter the cell
poor perfusion of coronaries ↓
Potassium leaks out of the cells
↓ ↓
hypoxia, metabolic acidosis hyperkalaemia, hyponatraemia and
hypocalcaemia
↓ ↓
Release of cardiac depressants intracellular lysosomes break down
↓
Cardiac (pump) failure SICK CELL SYNDROME
General clinical features
Stages of shock
1. Compensatory shock
2. Decompensatory shock
3. Irreversible shock
Cascade responses
Adrenergic response

Constriction of the venules and small veins,

vascular sphincters in the kidneys, splanchnic viscera and in the skin
↓
heart rate ↑
↓
blood to the right atrium and ventricle ↑
↓
pulmonary vasculature ↑
↓
left ventricular stroke volume ↑
sucks blood from extra thoracic sites to the heart and lungs.
filling of left ventricle and also its stroke volume
 Renin From the juxtaglomerular apparatus
↓
angiotensin I from the liver,
↓
Angiotensin II by the lungs
↓
selectively constricts the vasculature of the splanchnic organs, kidneys
and the skin
• Vasopressin is released due to stimulus from the baroreceptors
• Epinephrine is also vasoactive hormone which is released from the
adrenal medulla
• Collapse :
displaces blood from the lower part of the body to the heart and
increased cardiac output.
• to decrease of the capillary intravascular hydrostatic pressure.
• influx of water, sodium and chloride from interstitial tissue space into
the capillaries
• Epiephrine – Medulla
• Cortisol – cortex
• Glucagon – pancreas GLUCOSE ↑
• Insulin inhibition

• Hyperosmolarity
• Draw fluid from cells
Renal conservation
• Adreno corticotropic hormone + Angiotensin II → Aldosteron synthesis
Characteristic features
 Septic shock
• Gram-negative septic shock - Due to endotoxins
I. Strangulated Intestines,
II. Peritonitis,
III. Gastrointestinal Fistulas,
IV. Biliary And Urinary Infections,
V. Pancreatitis,
VI. Major Surgical Wounds,
VII. Diabetic Wounds,
VIII. Crush Injuries.
• Gram-positive septic shock
• Due to exotoxin by gram +ve bacteraemia like Clostridium tetani/welchii,
staphylococci, streptococci, pneumococci
• Fluid loss, hypotension is common; with normal cardiac output.
Pathophysiology of septic shock
Toxins/endotoxins from organisms
↓
Inflammation, cellular activation of macrophages, neutrophils, monocytes
↓
Release of cytokines, free radicals
↓
Chemotaxis of cells, endothelial injury, altered coagulation cascade—SIRS
↓
Reversible hyperdynamic warm stage of septic shock with fever, tachycardia, tachypnoea
↓
Severe circulatory failure with MODS (failure of lungs, kidneys, liver, heart) with DIC
↓
Hypodynamic, irreversible cold stage of septic shock.
Stages of septic shock
1. Hyperdynamic (warm) shock:
1. This stage is reversible stage.
2. Patient is still having inflammatory response, presents with
3. fever, tachycardia, and tachypnea, Pyrogenic response.
b. Hypodynamic hypovolaemic septic shock (cold septic shock):
• Patient is in decompensated shock.
• It is an irreversible stage along with MODS with
• anuria, respiratory failure (cyanosis), jaundice, cardiac depression, pulmonary
oedema, hypoxia, drowsiness, eventually coma and death occurs (Irreversible
stage).
 Traumatic shock
• Major fractures
• Crush injuries
• Extensive soft tissue injury
• Intra-abdominal injuries
Pathophysiology of Traumatic shock
Trauma
↓
Activates coagulation
↓
Micro thrombi release
↓
Occluded at pulmonary vasculature
↓
Resistance increases
↓
Rt. Ventricular diastolic pressure↑
 Neurogenic shock
• Paraplegia
• Quadriplegia
• Trauma to spinal cord
• Spinal anesthesia
Pathophysiology of Neurogenic shock
Dilatation of systemic vasculature
↓
Systemic arterial pressure
↓
Blood pools at systemic veins, venules
↓
Rt. Heart filling
Stroke volume
↓
Pulmonary blood volume
↓
Lt. heart filling
 Vasovagal shock
Dilatation of peripheral vascular system – lower limb, splanchnic bed
↓
Preload ↓
↓
Cardiac output ↓
↓
Bradycardia
↓
Blood flow to brain ↓
↓
Cebral hypoxia
↓
Unconsciousness
 ANAPHYLACTIC SHOCK
Causes : Penicillins, anaesthetics, stings, venom, shellfish

Antigens +IgE of mast cells and basophils

↓
histamine release
↓
large amount of SRS-A (Slow releasing substance of anaphylaxis).
C/F :
• Bronchospasm, laryngeal oedema
• Generalised rashes and oedema
• Hypotension, feeble pulse
COMPLICATIONS IN SHOCK
• ARDS and respiratory failure
• Acute Renal failure
• Stress ulcers, ileus, liver failure
• DIC, thrombocytopenia
• SIRS, MODS
 INVESTIGATIONS IN SHOCK
• Regular monitoring of BP, pulse, Heart rate. But in young patients and patients on beta
blockers, tachycardia may be masked.
• Respiratory rate.
• CVP line (Central venous pressure).
• PCWP (Pulmonary capillary wedge pressure).
• Pus, urine, blood culture in case of septic shock.
• U/S, CT, X-ray depending on location of pathology or septic focus.
• Measurement of urine output.
• Arterial PO2 and PCO2 analysis.
• Electrolyte estimation.
• Blood CBC, pH assessment, pulse oximetry.
• Activated partial thromboplastin time (APTT)
• Serum lactate estimation
Management
General treatment
1. Resuscitation
2. Control the bleed
3. ECF replacement
4. Drugs
I. Sedatives
II. Chronotropic
III. Intropics
IV. Vasodilators
V. Vasoconstrictor
 HYPOVOLEMIC SHOCK
• Pre hospital care
1. Immobilize
2. Splint – fracture
3. Adequate airway
• Emergency department care
1. Maximize oxygen delivery
2. Control the bleed
3. Rapid and appropriate disposition
 HYPOVOLEMIC SHOCK….
• CPR
• Pressure bandage
• Trendelenburg's position
• Keep warm
• Long bone fractures - traction
• Lost pulse in the emergency department or just prior to arrival,
• an emergency thoracotomy
• cross clamping of the aorta,
 HYPOVOLEMIC SHOCK…..
• In the patient with GI bleeding, IV vasopressin and H-2 blockers have
been used.
• In patients with variceal bleeding, a Sengstaken-Blakemore tube can
be considered

Complications:
• Esophageal Rupture,
• Asphyxiation,
• Aspiration And
• Mucosal Ulceration
 CARDIOGENIC SHOCK
• Oxygenation
• Intubation
• Cardioversion
• Dobutamine, Dopamine, epinephrine, norepinephrine, amrinone, milrinone
• Anticoagulants
• Thrombolytics
• Beta blockers
• Nitrates
• Percutaneous trans luminal coronary angioplasty
• CABG
• Intra Aortic balloon pump
SEPTIC SHOCK ANAPHALYCTIC

3rd generation antibiotics Adrenaline 100ug IV,

Ceftazimide
Amikacin
Cefoperazone
 Normal values
Index

2.6–4.2 L/min/m2

SI = HR/Systolic BP 0.5-0.7

MSI ≥ 1.3 was a strong

Modified SI = HR/Mean arterial pressure predictor of in hospital and
6-month mortality among
patients with STEMI.
Thank you