SHOCK H.A MWAKYOMA, MD

Approach to study: Definition of shock Classification of shock Causes of shock Pathogenesis of cardiac, neurogenic, septic & anaphylactic shock Stages of shock including compensatory mechanisms Clinical features of shock (at each stage) Morphology of various organs & tissues in shock

What is shock? Shock is the clinical syndrome that results from inadequate tissue perfusion

Circulatory Homeostasis Tissue perfusion is driven by blood pressure BP = CO X PVR CO – Cardiac Output PVR – Peripheral Vascular resistance

Cardiac Output CO = SV X HR BP= SV X HR X PVR This means that Blood Pressure = Stroke Volume X Heart Rate X Peripheral Vascular Resistance

What affects Stroke volume? Volume of Blood pumped by the heart during 1 cycle What affects Stroke volume? Rhythm Problems Blood Volume Stroke Volume Heart Muscle Damage MechanicalObstruction Mechanical Obstruction

Classification of shock Cardiogenic, due to heart failure Hypovolemic (oligemic), due to fluid or blood loss Distributive (hypotensive) owing to peripheral vasodilation

Types of Shock Hypovolemic Cardiogenic Neurogenic Anaphylactic Septic Redistributive shock

Redistributive Decreased Peripheral Vascular Resistance Septic Shock Spinal / Neurogenic Shock ANAPHYLACTIC shock

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? Insufficient delivery of oxygen & nutrients to cells and tissues. Inadequate clearance of metabolites.

Outcomes of cellular hypoxia Shift from aerobic to anaerobic metabolism. This results in increased lactate production and later on, lactic acidosis.

Outcomes of cellular hypoxia 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 use Tissue perfusion Impaired cellular metabolism Anaerobic metabolism Stimulation of clotting cascade & inflammatory response Impaired glucose usage ATP synthesis  Intracellular Na+ & water Na+ Pump Function Cellular edema  Vascular volume

Hypovolemic Shock Decreased intravascular volume Causes: Hemorrhage external internal GI tract hemothorax peritoneal or retroperitoneal space Loss of fluid into third space burns pancreatitis

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

Renin-Angiotensin-Aldosterone Plasma volume Kidney (juxtaglomerular apparatus) Detected by &/Or  [Na+] Releases Renin Via ACE (Angiotensin Converting Enzyme) Angiotensin II… Angiotensinogen Angiotensin I… Converts

Pathophysiological Response “Flight or fight response” Increased Catecholamine release Activation of Renin-Angiotensin system Increase glucocorticoid and mineralcorticoid release Activation of Sympathetic nervous system

Cardiogenic Shock Myocardial pump failure Extrinsic compression myocardial infarction myocardial rupture cardiac arrhythmia Extrinsic compression cardiac tamponade Outflow obstruction(Obstructive heart failure) pulmonary embolus valvular disease (Aortic stenosis)

Cardiogenic Shock Catecholamine R.A.S.  CO Release Activation  SVR Impaired myocardial function  SVR Volume/ Preload Myocardial O2 demand O2 supply Peripheral & pulmonary edema  Dyspnea

Anaphylactic Shock Caused by a hypersensitivity reaction to an allergen in a previously sensitised patient

Anaphylactic Shock Massive & systemic allergic reaction Large release of histamine Increases membrane permeability & vasodilation

Common Features Angio-oedema Bronchoconstriction Vasodilatation and hypotension Urticareal rash

Common Features Angio-oedema Bronchoconstriction Vasodilatation and hypotension Urticareal rash

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

Effects of cytokine release

Effects Of Lipopolysaccharide (LPS) And Secondarily Induced Effector Molecules

MODS= Multiple organ dysfunction syndrome

Multiple Organ Dysfunction System Progressive dysfunction of two or more organ systems Caused by uncontrolled inflammatory response to injury or illness Typically sepsis

STAGES OF SHOCK Nonprogressive stage (compensated phase) Progressive stage (Decompensated phase) Refractory stage (irreversible)

Features of compensated shock Tachycardia Skin pallor due to constriction of arterioles Reduced urine production

Decompenstated Shock Defense mechanisms begin to fail Presentation Hypotension Marked increase in heart rate Rapid, thready pulse Agitation, restlessness, confusion

Features of decompenstaed but still reversible shock CONT-- Dyspnoea & tachypnoea Pulmonary oedema slowly develops, further worsening hypoxia Oliguria (urine volume<500ml/24hr) Acidosis due to anaerobic glycolysis

Irreversible Shock Complete failure of compensatory mechanisms Death even in presence of resuscitation

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 (Disseminated Intravascular coagulation)

Symptoms of Shock Anxiety /Nervousness General Symptoms Specific Symptoms 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)

Signs of Shock Pallor Cold and clammy extremities Sweating Cyanosis Tachypnoea Tachycardia Confusion & agitation Stridor Hypotension Loss of consciousness

Clinical Course Hypovolemic shock Cardiogenic shock and septic 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)

Clinical Course Hypovolemic shock Cardiogenic shock and septic 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

Myocardial necrosis(coagulation necrosis)

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.

Markedly congested & heavy lung

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.

Mortality rate of ARDS is high (60%).