Common types of shock: –Cardiogenic shock –Hypovolemic shock –Septic shock
Less common types of shock Neurogenic shock Anaphylactic shock Hypoadrenal shock
Common factor Circulatory collapse resulting from a disproportion between circulating blood volume & the vascular space that it has to fill. The ensuing tissue hypoxia or anoxia leads to multiple organ failure.
What happens with the perfusion deficit? 1.Insufficient delivery of oxygen & nutrients to cells and tissues. 2.Inadequate clearance of metabolites.
Outcomes of cellular hypoxia 1.Shift from aerobic to anaerobic metabolism. 2.This results in increased lactate production and later on, lactic acidosis.
The metabolic & hemodynamic derangements are correctible at the outset & are associated with reversible cell injury. Persistence or worsening of the shock state leads to irreversible injury and death of cells and possibly, death of the patient.
Cellular Response to Shock Tissue perfusion perfusion Na + Pump Function Function ATP synthesis synthesis AnaerobicmetabolismAnaerobicmetabolism Cellular edema Vascular volume Cellular edema Vascular volume Impaired cellular metabolism metabolism O 2 use use Intracellular Na + Intracellular Na + & water Intracellular Na + Intracellular Na + & water ImpairedglucoseusageImpairedglucoseusage Stimulation of clotting cascade & inflammatoryresponse Stimulation of clotting cascade & inflammatoryresponse
Cardiogenic Shock CO R.A.S.ActivationR.A.S.Activation Dyspnea O 2 supply supply Volume/ Preload Preload SVR Peripheral & pulmonary edema Peripheral & pulmonary edema Impaired myocardial function Impaired Myocardial O 2 demand Myocardial O 2 demand Catecholamine Release Release
Neurogenic Shock Sympathetic Tone Or Parasympathetic Tone Sympathetic Tone Or Parasympathetic Tone Vascular Tone Massive Vasodilation SVR & Preload Cardiac Output Tissue perfusion perfusion
Anaphylactic Shock Massive & systemic allergic reaction Large release of histamine Increases membrane permeability & vasodilation
Anaphylactic Shock Caused by a hypersensitivity reaction to an allergen in a previously sensitised patient
Septic Shock “Circulatory failure” Due to systemic infection
Septic Shock Leading cause of death in intensive care units Most cases (70%) are caused by gram negative bacteria (LPS-lipopolysaccharide) Also can occur with gram positive bacteria and fungal organisms
Homeostatic Mechanisms in Shock Baroreceptor reflexes and catecholamine release –maintain cerebral and cardiac perfusion –decrease perfusion to gut, skin and kidneys Activation of renin-angiotensin system –angiotensin II constricts efferent arteriole of glomerulus to maintain GFR –aldosterone promotes sodium retention Release of Arginine Vasopressin (ADH) –promotes renal conservation of water
Symptoms of Shock Anxiety /Nervousness Dizziness Weakness Nausea & Vomiting Thirst Confusion Decreased Urine Output History of Trauma / other illness Vomiting & Diarrhoea Chest Pain Fevers / Rigors Shortness of breath (stridor) General SymptomsSpecific Symptoms
Signs of Shock Pallor Cold and clammy extremities Sweating Cyanosis Tachypnoea Tachycardia Confusion & agitation Stridor Hypotension Loss of consciousness
Features of compensated shock Tachycardia Skin pallor due to constriction of arterioles Reduced urine production
Features of decompenstaed but still reversible shock Hypotension Dyspnoea & tachypnoea Pulmonary oedema slowly develops, further worsening hypoxia Oliguria (urine volume<500ml/24hr) Acidosis due to anaerobic glycolysis
Features of irreversible shock Marked hypotension with extreme tachycardia (filiform pulse) Respiratory distress which is not responsive to oxygen therapy & assisted ventilation Loss of consciousness progressing to coma Gastrointestinal bleeding Anuria with elevated BUN & creatinine Severe acidosis Laboratory & clinical signs of DIC
Clinical Course Hypovolemic shock –If patient is young and healthy, most survive if resuscitation restores perfusion Cardiogenic shock and septic shock –Up to 75% mortality even with best care Patients succumb with multi-organ failure –Tubular necrosis of kidneys –Ischemic enteropathy –Disseminated intravascular coagulation –Acute respiratory distress syndrome (septic shock)
Morphology of Shock Hypoxic injury to multiple organs Kidneys –medulla and tubules most affected –acute tubular necrosis Gastrointestinal tract –mucosa most sensitive to hypoxia Brain Heart –subendocardial necrosis of myocardium Lungs –resistant to hypoxia but involved with septic shock
Kidney in shock:Coagulation necrosis of tubules
Renal Biopsy in DIC Capillary loops of glomeruli occluded by fibrin thrombi. H&E stain on left and MSB (Martius scarlet blue) for fibrin on the right
Adult respiratory syndrome (ARDS) Synonyms: –Shock lung –Diffuse alveolar damage –Acute alveolar injury –Traumatic wet lungs These are descriptive terms for a syndrome caused by diffuse alveolar capillary damage.
Clinically characterized by: Rapid onset of severe life-threatening respiratory insufficiency Cyanosis Severe arterial hypoxemia that is refractory to oxygen therapy Frequently progresses to extrapulmonary multisystem organ failure.
Some causes of ARDS: Shock Sepsis Extensive surface burns Massive fractures & other trauma
Morphology: In the acute edematous stage, the lungs are heavy, firm & boggy due to congestion, edema & inflammation.
Microscopy Alveoli are lined by waxy hyaline membranes.
This is followed by: Proliferation of type II pneumocytes. However resolution does not usually occur. More commonly, there is organization of the fibrin exudate, with resultant intra-alveolar fibrosis. There is marked thickening of the alveolar septae.
Approach to study: 1.Definition of shock 2.Classification of shock 3.Causes of shock 4.Pathogenesis of cardiac, neurogenic, septic & anaphylactic shock 5.Stages of shock including compensatory mechanisms 6.Clinical features of shock (at each stage) 7.Morphology of various organs & tissues in shock