Pathophysiology of shock

pathophysiology of shock in detail,types of shock

1. G.P.Chakravarthy Moderator - Dr.Ranjith M.S Pathophysiology of shock

2. introduction Definition : A modern definition and approach to shock acknowledges that shock consists of inadequate tissue perfusion marked by decreased delivery of required metabolic substrates and inadequate removal of cellular waste products

3. Types of shock Hypovolemic Distributive ( septic,neurogenic,anaphylactic ) Cardiogenic Obstructive

4. Hypovolaemic shock Due to loss of blood , plasma ,body water and electrolytes Often due to haemorrhage ,vomitings,diarrhoea Characteristics : decreased systemic arterial pressure(low bp ) tachycardia, increased vascular resistance(cold clammy extrimities )

5. pathophysiology Hemorrhage /capillary leakage Decreased filling of rt heart Decreased filling of lt atrium & ventricle Drop in SV & arterial BP

6. pathophysiology Compensatory mechanisms : 1. ADRENERGIC DISCHARGE : Starts within 60 secs after blood loss Constriction of venules & small veins Increase in diastolic pressure of RV and inc in SV Inc in LV fillings and LV stroke volume Adrenergic discharge causes selective vasoconstriction – in splanchnic viscera,kidneys,skin

7. pathophysiology Compensatory mechanisms: 2.HYPERVENTILATION : Shortly after hemorrhage there will be met.acidemia Spont . Deep breathing sucks blood into heart & lungs Increase in stroke volume of LV Hyperventilation occurs within 60 secs

8. pathophysiology Compensatory mechanisms : 3.release of vasoactive harmones : Low perfusion to kidneys baroreceptors adr.medulla Activation of RAAS VASOPRESSIN ADRENALINE Potent selective systemic vaso vasoconstr . Vasoconstrictor constrictor All these divert blood from kidneys,spl.organs,skin to brain & heart

9. pathophysiology Compensatory mechanisms : 4.collapse : Assumption of recumbent posture displaces blood from lower ext. to heart – increases C.O 5.renal conservation of body fluids : Any stress (shock) angiotensin II aldosterone ( adr.cortex ) Resorption of sodium and water (maintain I.V.volume )

10. pathophysiology Compensatory mechanisms : 6.Resorption of fluid from intracellular to interstitium : Epinephrine cortisol glucagon inhibitn of insulin High extra cellular glucose conc & products of anaerobic met. Accumulate in ecf hyperosm . Of ECF ( interstitium ) Draws fluid from ICF to ECF ( interstitium )

11. pathophysiology Compensatory mechanisms : 7.Resorption of fluid from interstitial tissue : adrenergic discharge Constriction of arterioles,precapillay postcapillary venules,small veins of skin & skeletal muscles Decrease in capillary intravascular hydrostatic pressure Influx of Na,water,Cl from interstitium to capillaries (I.V)

12. COMPENSATORY MECHANISMS

13. PATHOPHYSIOLOGY

14. PATHOPHYSIOLOGY AT CELLULAR LEVEL : deprivation of O2 anerobic metabolism accumulation of lactic acid – met.acidosis when glu is exhausted – anaerobic also stops failure of Na/K pumps - intracellular lysosomes activate release autodigestive enzymes – cell lysis

15. Stages/severity of shock Compensated shock : In compensated shock , there is adequate compensation to maintain central blood volume and preserve flow to the kidneys, lungs and brain . tachycardia and cool peripheries there may be no other clinical signs There is a systemic metabolic acidosis within the underperfused organs. Although clinically occult, this state will lead to multiple organ failure and death if prolonged

16. Stages/severity of shock Decompensated shock : Further loss of circulating volume overloads the body’s compensatory mechanisms and there is progressive renal, respiratory and cardiovascular decompensation .

17. Stages/severity of shock

18. Septic shock May be due to gram positive( clostridium,staph,strept,pneumo ),gram negative ( e.coli,klebsiella,proteus ), fungi,viruses Gram negative septic shock is also referred as endotoxic shock Typically it is vasodilatory shock causing hypotension – resistant to vasopressors Because endotoxin induces release of isoform of NO synthetase which causes sustained prolonged release of NO

19. Septic shock Pathophysiology : endotoxin & other microbial products Complement neutrophil&macrophage Activation endothelial cell activation activation ( cytokines,free radicals) Procoagulants NO,IL, reactive o2 species systemic effects Microvascular vasodiation,inc permeability met.abnormalities Thrombosis(DIC) decreased perfusion Tissue ischemia MULTI ORGAN FAILURE

20. Septic shock Stages 1.hyperdynamic shock (reversible stage): Fever,tachycardia,tachypnoea Pyrogenic response is still intact 2.hypodynamic shock (irreversible): Pyrogenic response is lost Decompensated shock Present with MODS with anuria,cyanosis (respiratory failure),pulmonary edema,liver failure (jaundice),cardiac depresion Eventually coma and death

21. Neurogenic shock D iminished tissue perfusion as a result of loss of vasomotor tone to peripheral arterial beds . Causes of neurogenic shock : Spinal cord trauma Spinal cord neoplasm Spinal/epidural anesthetic

22. Neurogenic shock Sympathetic input to the heart, which normally increases heart rate & cardiac contractility, I nput to the adrenal medulla, which increases catecholamine release, may also be disrupted , preventing the typical reflex tachycardia that occurs with hypovolemia

23. Neurogenic shock Acute spinal cord injury results in activation of multiple secondary injury mechanisms: ( a) vascular compromise to the spinal cord with loss of autoregulation , vasospasm, and thrombosis (b ) loss of cellular membrane integrity and impaired energy metabolism (c ) neurotransmitter accumulation and release of free radicals . Importantly, hypotension leads to further reduction in blood flow to spinal cord worsening acute spinal cord injury

24. Neurogenic shock The classic description of neurogenic shock consists of Decreased blood pressure associated with bradycardia (absence of reflexive tachycardia due to disrupted sympathetic discharge) Warm extremities (loss of peripheral vasoconstriction ), motor and sensory deficits indicative of a spinal cord injury, Radiographic evidence of a vertebral column fracture

25. Cardiogenic shock Cardiogenic shock is defined clinically as circulatory pump failure leading to diminished forward flow and subsequent tissue hypoxia , in the setting of adequate intravascular volume . Hemodynamic criteria include sustained hypotension (i.e., SBP <90 mmHg for at least 30 minutes), reduced cardiac index (<2.2 L/min per square meter), and elevated pulmonary artery wedge pressure (>15 mmHg)

26. Cardiogenic shock Causes of cardiogenic shock Acute myocardial infarction Pump failure Acute mitral regurgitation Acute ventricular septal defect Free wall rupture Pericardial tamponade Arrhythmia End-stage cardiomyopathy Myocarditis Severe myocardial contusion Left ventricular outflow obstruction Aortic stenosis Hypertrophic obstructive cardiomyopathy Obstruction to left ventricular filling

27. Cardiogenic shock Pathophysiology Diminished cardiac output or contractility in the presence of adequate intravascular volume Underperfused vascular beds Increased sympathetic stimulation of the heart Increases heart rate, myocardial contraction, and myocardial O2 consumption

28. Cardiogenic shock Pathophysiology coronary artery blood flow is not increased in patients with fixed stenosis of the coronary arteries . resulting in a scenario of increased myocardial O2 demand Results in Acute heart failure fluid accumulation in the pulmonary microcirculatory bed, decreasing myocardial O2 delivery even further. Resulting in cardiogenic shock

29. Obstructive shock Due to mechanical obstruction of venous return I n trauma patients, this is most commonly due to the presence of tension pneumothorax Causes Pericardial tamponade Pulmonary embolus Tension pneumothorax IVC obstruction (Gravid uterus on IVC) Deep venous thrombosis Neoplasm

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