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SHOCK:

DR. N.K.JAIN ASSISTANT PROFESSOR DEPTT. Of Surgery SHOCK

Objectives:

Define shock and its different categories Review basic physiologic and pathophysiologic aspects of shock Objectives

Definition of Shock:

Inadequate tissue perfusion to meet tissue demands . Usually result of inadequate blood flow and/or oxygen delivery Circulatory failure is a life-threatening medical condition that occurs due to inadequate substrate for aerobic cellular respiration . In the early stages this is generally an inadequate tissue level of oxygen . Shock is not a blood pressure diagnosis Definition of Shock

Hypotension:

In Adults: systolic BP  90 mm Hg mean arterial pressure  60 mm Hg  systolic BP > 40 mm Hg from the patient’s baseline pressure Hypotension

Pathophysiology of shock:

Oxygen Demand > Supply Pathophysiology of shock

Slide 6:

COMPONENTS OF THE C.V.S. THE HEART (pump) THE BLOOD (circulating fluid) THE VASCULAR CAPACITY (veins and arteries) THE MICRO- CIRCULATION

Mechanical Requirements for Adequate Tissue Perfusion:

Fluid Pump Vessels Flow Mechanical Requirements for Adequate Tissue Perfusion

Pathophysiology:

ATP + H 2 O  ADP + P i + H + + Energy Acidosis results from the accumulation of acid when during anaerobic metabolism the creation of ATP from ADP is slowed. H + shift extracellularly and a metabolic acidosis develops Pathophysiology

Understanding Shock:

Cellular responses to decreased systemic oxygen delivery ATP depletion → ion pump dysfunction Cellular edema Hydrolysis of cellular membranes and cellular death Goal is to maintain cerebral and cardiac perfusion Vasoconstriction of splanchnic, musculoskeletal, and renal blood flow Leads to systemic metabolic lactic acidosis that overcomes the body’s compensatory mechanisms Understanding Shock

Slide 10:

DO2 O2 CASECADES HEMO DYNAMICS VENTILATION PULMONARY O2 EXCHANGE O2 TRANSPORT TISSUE EXCHANGE QT HB CONTENT MICR CIRCULATION QT x HB x 10 x 1.36 X SO2 + PO2 x0.003

Slide 11:

TISSUE PERFUSION CONSTANT FLOW CONSTANT DO2 TARGET FUNCTION OF CVS REGIONAL PERFUSION PRESSURE

Slide 12:

P = F X R Autorgulation is controlled by; *** Myogenic *NO *** Metabolic *H Ione *ADENOSINE *CO2 *PG *O2 F P R P R F F CONSTANT TISSUE PERFUSION MAP=60mmHg Tissue perfusion

Slide 13:

Large arteries Resistant arteriole Precapillary arteriole Capillary Post capillary venule Collecting vein Capacitance vein MAP R F BP Constriction Dilatation Constant Constriction Constriction Dilatation Constant Constriction BP MAP<60 Constriction no more Flow Constriction = x

Slide 14:

REGIONAL PERFUSION PRESSURE MAP QT SVR MAP = QT X SVR

Slide 15:

BODY RESPONSE TO SHOCK Neuro endocrinal Aortic arch, carotid body, cerebral ischemia, renal ischemia Catecholamine ADH, RAAS, STEROIDS Vasoconstriction Salt and water retention To keep regional perfusion pressure Vasodilatation To keep organ flow constant P = F X R MAP 60 mmHg TISSUE PERFUSION P = F X R

Determinants of Oxygen Delivery:

Oxygen content = 1.34 ( Hgb x SaO2) + (PaO2 x 0.003) SaO2: Oxygen saturation Hgb : Hemoglobin concentration PaO2: partial pressure Oxygen in plasma To improve Oxygen content Increase Hemoglobin concentration Increase saturation Determinants of Oxygen Delivery

Determinants of Oxygen Delivery:

Cardiac output C.O. = Heart rate x stroke volume To improve Cardiac output Increase Heart rate Increase Stroke Volume Preload – volume of blood in the ventricle Afterload – resistance to contraction Contractility – force applied Determinants of Oxygen Delivery

Slide 18:

Compensatory mechanisms for shock 1 ** S.V.R. vascular capacity Spasm of large and resistant arteries Catecholamine Vasopressin Angiotensin 2 Cortisol Aldosterone 2 ** QT Effective blood volume x = BP (MAP> 60mmHg) *Venous spasm to V.R. *Salt retention Aldosterone * Water retention ADH *Stimulation of thirst Ag.2 *Decrease hydrostatic cap .P. Tissue fluid reabsorption at rate 15 ml/ kg /h Target point Mediators

Shock -- Classification:

Weil and Shubin in 1972 classification Four major categories Hypovolemic Cardiogenic Extracardiac Obstructive Distributive Overlap exists, and also concomitant categories exist Shock -- Classification TYPES OF SHOCK

Classification of Shock:

Compensated Organ perfusion is maintained Uncompensated Circulatory failure with end organ dysfunction Irreverisble Irreparable loss of essential organs Classification of Shock

Hypovolemic Shock:

#1 cause of death world wide Gastroenteritis Hemorrhagic – Trauma, GI bleed Hypovolemic Shock

Slide 23:

THE BLOOD WHOLE BLOOD EXTERNAL HG. INTERNAL HG. PLASMA GUT *VOMITING *NGT. DRAIN * DIARRHOEA * FISTULA SKIN SWEAT * BURN KIDNEY *DM *DI *DIURETIC 3 rd SPACE * ASCITES

Classes of Hypovolemic Shock:

Classes of Hypovolemic Shock

Diagnosis of Hypovolemic Shock:

Early Increase HR Decrease perfusion Normal BP, decrease pulse pressure Late Sign increase HR Sign decrease perfusion Decrease BP End organ dysfunction Diagnosis of Hypovolemic Shock

Cardiogenic Shock:

Pump failure/malfunction (decreased contractility) Cardiogenic Shock

Causes:

Myocardial Infarction, contusion, myocarditis, cardiomyopathy, pharmacologic, depressant factors Mechanical Valvular stenosis, regrurgitation Septal Defects Arrhythmogenic Causes

Slide 29:

CARDIAC CAUSES AFTERLOAD PRELOAD VALVES MUSCLE POWER RATE& RHYTHEM

Cardiogenic Shock Symptoms:

Tachycardia Tachypnea Respiratory distress Mental status change Cool extremities Poor perfusion Signs of dehydration Cardiogenic Shock Symptoms

Shock -- Classification --Obstructive:

Extrinsic Vascular Compression tumors, fibrosis Increased Intrathoracic Pressure Tension pneumo; high autopeep in PPV Flow obstruction PE, Air embolism, tumors, Ao dissection, Ao coarctation, acute pulmonary HTN, tamponade. Shock -- Classification --Obstructive

Obstructive Shock:

Obstructive Shock

Obstructive Shock:

Tension pneumothorax Air trapped in pleural space with 1 way valve, air/pressure builds up Mediastinum shifted impeding venous return Chest pain, SOB, decreased breath sounds No tests needed! Rx: Needle decompression, chest tube Obstructive Shock

Obstructive Shock:

Cardiac tamponade Blood in pericardial sac prevents venous return to and contraction of heart Related to trauma, pericarditis, MI Beck’s triad: hypotension, muffled heart sounds, JVD Diagnosis: large heart CXR, echo Rx: Pericardiocentisis Obstructive Shock

Obstructive Shock:

Pulmonary embolism Virscow triad: hypercoaguable , venous injury, venostasis Signs: Tachypnea, tachycardia, hypoxia Low risk: D-dimer Higher risk: CT chest or VQ scan Rx: Heparin, consider thrombolytics Obstructive Shock

Shock -- Classification --Distributive:

SIRS-related As sepsis (infectious); pancreatitis; trauma; burns. Anaphylactic/ anaphylactoid Spinal Trauma (low pulse, SVR low) Toxic, pharmacologic (B-blockers overdose) Endocrine (thyroid, adrenal crisis) Shock -- Classification --Distributive

Distributive Shock:

Abnormal vessel tone (decreased afterload) Distributive Shock

Distributive Shock:

Vasodilitation Venous Pooling Decreased Afterload Maldistribution of regional blood flow Distributive Shock

Distributive Shock:

Neurogenic or Anaphylactic Shock Diminished or absent sympathetic tone Reduce peripheral vascular tone Peripheral pooling of blood volume Inadequate venous return Decreased perfusion, acidosis, hypotension Distributive Shock

Anaphylactic Shock:

Anaphylaxis – a severe systemic hypersensitivity reaction characterized by multisystem involvement IgE mediated Anaphylactoid reaction – clinically indistinguishable from anaphylaxis, do not require a sensitizing exposure Not IgE mediated Anaphylactic Shock

Anaphylactic Shock:

What are some symptoms of anaphylaxis? Anaphylactic Shock First- Pruritus, flushing, urticaria appear Next- Throat fullness, anxiety, chest tightness, shortness of breath and lightheadedness Finally- Altered mental status, respiratory distress and circulatory collapse

Anaphylactic Shock:

Risk factors for fatal anaphylaxis Poorly controlled asthma Previous anaphylaxis Reoccurrence rates 40-60% for insect stings 20-40% for radiocontrast agents 10-20% for penicillin Most common causes Antibiotics Insects Food Anaphylactic Shock

Anaphylactic Shock:

Mild, localized urticaria can progress to full anaphylaxis Symptoms usually begin within 60 minutes of exposure Faster the onset of symptoms = more severe reaction Biphasic phenomenon occurs in up to 20% of patients Symptoms return 3-4 hours after initial reaction has cleared A “lump in my throat” and “hoarseness” heralds life-threatening laryngeal edema Anaphylactic Shock

Anaphylactic Shock- Diagnosis:

Clinical diagnosis Defined by airway compromise, hypotension, or involvement of cutaneous, respiratory, or GI systems Look for exposure to drug, food, or insect Labs have no role Anaphylactic Shock- Diagnosis

Neurogenic Shock :

Occurs after acute spinal cord injury Sympathetic outflow is disrupted leaving unopposed vagal tone Results in hypotension and bradycardia Spinal shock- temporary loss of spinal reflex activity below a total or near total spinal cord injury (not the same as neurogenic shock, the terms are not interchangeable) Neurogenic Shock

Neurogenic Shock :

Loss of sympathetic tone results in warm and dry skin Shock usually lasts from 1 to 3 weeks Any injury above T1 can disrupt the entire sympathetic system Higher injuries = worse paralysis Neurogenic Shock

Septic Shock:

Terminology in Sepsis Infection = response to micro organism Bacteremia = bug in blood Systemic Inflammatory Response Syndrome (SIRS) T>38, <36 Increase HR Increase RR, paCO2<32 WBC>12,000, <4,000, >10% bands Septic Shock

Septic Shock:

Terminology in Sepsis Sepsis = SIRS as response to a known infection Severe sepsis = Sepsis + organ dysfunction Septic Shock = Sepsis + inadequate oxygen delivery Multiple Organ Dysfunction Syndrome (MODS) – organ dysfunction that requires intervention Septic Shock

Septic Shock:

Components of Septic shock Decreased volume Decreased pump function Abnormal vessel tone Septic Shock

Septic Shock:

Therapy for Caridovascular Support Preload Volume Contractility Inotropes Afterload Vasodilators Septic Shock

Septic Shock:

Etiologies Inflammatory: too much, too little Coagulation pathway: DIC-bleeding, pro-coagulant, microthombosis Multiple organ system failure Septic Shock

Recognition of Septic Shock:

Early – warm shock – similar to neurogenic shock Late – Cold shock – similar to cardiogenic shock Recognition of Septic Shock

Early vs Late Septic Shock:

Early vs Late Septic Shock Early Late Heart rate Tachycardia Tachycardia/ bradycardia Blood pressure Normal decreased Peripheral Perfusion Warm/cool Dec./inc. pulses Cool Dec. pulses

Early vs Late Septic Shock:

Early vs Late Septic Shock Early Late End-organ: skin Dec. cap refill Very dec. cap Refill Brain Irritable, restless Lethargic, unresponsive Kidneys Oliguria Oliguria, anuria

Slide 57:

HYPOXIC FAILURE COMPENSATORY POST CAP.VASO-CON. STRESS PRE&POST CAP.V.CON. PRECAPILLARY SHUNT FAILURE OPEN PRECAP LEAKAGE RECOVARY

Summary:

Type PAOP C.O. SVR HYPOVOLEMIC    CARDIOGENIC    DISTRIBUTIVE  or N varies  OBSTRUCTIVE    Summary

Slide 59:

SEQULEE OF SHOCK INSULT MILD Within the adaptive mechanisms Moderate To severe Beyond the adaptive mechanisms Normal physiologic oscillation Pathological oscillation Failure of compensatory mechanisms MAP<60 Failure of Autorgulation Tissue flow DO2 CEF OF O2 Tissue necrosis MSOD Death

Slide 61:

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