Name: D N Ezrinah Binti D N Esham

Roll No: 121303632
Group E1b Batch 32
SDL 1 : Shock
10/2/16

SHOCK
Definition:
shock is a state of low tissue perfusion which are inadequate or
the normal cellular respiration.
Pathophysiology:
1. Cellular:
Decrease tissue perfusion to the cell
Anaerobic respiration
Production of lactic acid

Failure

of Na+/K+ pumps
Metabolic acidosis

autodigestive

system release
Intracellular content
into the blood stream
2. Microvascular:
Hypoxia & acidosis state
Activate complement & neutrophils
Oxygen free radical & cytokine
Endothelial injury
Leaky vessels

neutrophils. haemorrhage.Fluid leaks out Tissue oedema 3. hypovolaemia Hypoxia and its effect . trauma. complement) flushed back into circulation Endothelial injury Multiple organ Failure Death Stages of shock: Factors like infection. Systemic: Tissue perfusion Reduce GFR Metabolic acidosis preload and afterload Urine output respiratory rate sympathetic Activation RAS activity Ventilation Catecholamine release Sodium-water reabsorption Tachycardia # Ischemia reperfusion syndrome    Further injury to the tissue which occur once normal circulation is restored Lactic acid and K+ load to: a) Myocardial depression Hypotension b) Vascular dilation The activated cellular & humoral response (platelet. burns.

Led to increase cytokine level. cardiomyopathy o Cardiac insufficiency may cause by drugs. diarrhea. altered complement activation.SIRS (Systemic Inflammatory Response Syndrome) s due to vasodilatation. lung. Hypovolemic shock o Due to reducing circulating volume o Hemorrhagic / non-hemorrhagic o Non hemorrhagic cause: dehydration. cardiac dysarrythmias. cellular dysfunction. failure to have a localization of inflammation. bacterial and humoral agents o Pt may resent with classical sign of shock + venous hypertension / systemic edema . DIC and pump failure. It is a severe form of reversible shock These will led to established microvascular occlusion. vomiting. abnormal NO synthesis. Classification of shock: 1. thrombosis. free radical production. MODS (multisystem organ failure)-irreversible shock of kidney. leukocyte migration and activation. liver. sickle cell syndrome. increased endothelial permeability.3rd spacing o Most common of shock 2. clotting system and brain. Cardiogenic shock: o Due to failure of heart to pump blood o Eg: myocardial infarction.

5. Obstructive shock: o Presence of decrease of preload due to mechanical obstruction of cardiac filling. Distributive shock o Type: a) Septic shock b) Anaphylactic shock c) Neurogenic shock o Anaphylactic shock: high output cardiac failure o In adrenal insufficiency: shock state due hypovolemia & poor response to exogenous catecholamine. altered coagulation cascade-SIRS Revesible hyperdynaic warm stage of shockwith fever. o Septic shock: Endotoxin Inflammation. endothelial injury. tachycardia.3. pulmonary embolism. tachypnea. tension pneumothorax. irreversible cold stage of septic shock. air embolus 4. Endocrine shock: o Present with combination of hypovolemic. o Cause: hypo/hyperthyroidism Adrenal insufficiency Severity of shock: . activation of cellular and humoral response Release of vasoactive substance Chemotaxis of cell. or distributive shock. Severe circulatory failure with MODS and DIC Hypodynamic. o Eg: cardiac tamponade. cardiogenic.

cardiac failure . Multiple organ failure: o Prolonged systemic ischemia and reperfusion injury o Define as 2 or more failed organ system o Organ involved: lung.acute lung injury Clotting-coagulopathy Cardiac. o Death 2. Unresuscitable shock: o loss of ability of body to compensate due to cellular ischaemia o there would be myocardial depression and loss of responsiveness to fluid and inotrophic drug o peripherally.compensat mild moderate severe ed + ++ ++ +++ acidosis Urine output Normal Consciousn Normal Normal Mild Reduced Drowsy Anuric Comatose ess Respiratory Normal anxiety Increase Increase Labored rate Pulse Mild Increase Increase Increase Blood increase normal Normal Mild Severe Lactic pressure hypotensio hypotesion n Consequences: 1. there Is loss to maintain systemic vascular resistance lead to further hypotension.