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Shock
- 1. SHOCK Dr. Janam SHRESTHA FCPSSurgery Trainee Chitwan Medical College Surgeons are the masters of fluids because they need to be
- 2. History • Ambroise Paré(1510-1590): urged the use of clysters (enemas to administer fluid into the rectum. • Miraculous deliverance of Anne Green -1650 • Herman(1830): 1st clear descriptions of intravenous (IV) fluid therapy. In response to a cholera epidemic, he attempted to rehydrate patients by injecting 6 ounces of water into the vein. • Crile (1899), using sphygmomanometers, proposed that a profound decline in blood pressure (BP) could account for all symptoms of shock.
- 3. Definition • Systemic stateof low tissue perfusion which is inadequate for normal cellular respiration. • insufficient delivery of oxygen and glucose cells switch from aerobic to anaerobic metabolism perfusion is not restored, cell death ensues.
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- 9. Shock – Effectson Organ • Heart – ↓ CO / hypotension / myocardial depressants • Lung - ↓gas exchange / tachypnoea / pulmonary edema • Endocrine – ADH → ↑ reabsorption of water • CNS – perfusion ↓ – drowsy • Blood - Coagulation abnormalities – DIC • Renal - ↓ GFR - ↓ urine output • GIT – mucosal ischaemia – bleeding & hepatic - ↑ enzyme levels
- 11. Clinical alterations inshock • The presentation of patients with shock may be Subtle (mild confusion, tachycardia) • Or easily identifiable(profound hypotesion.anuria) • The clinical manifestation of shock result from • 1- inadequate tissue perfusion and oxygenation • 2- Compensatory responses • 3- The specific etiology
- 12. Classification of Shock •Hypovolaemic shock (most common) • Cardiogenic shock • Obstructive shock • Distributive shock • Endocrine shock / Metabolic shock
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- 15. HYPOVOLAEMIC ETIOLOGY • Hemorrhagic • Non-hemorrhagic poor fluid intake (dehydration), excessive fluid loss due to vomiting, Fistula, diarrhoea, Burn urinary loss (eg. diabetes), evaporation, or ‘third-spacing’ where fluid is lost into the gastrointestinal tract and interstitial spaces, as for example in bowel obstruction or pancreatitis
- 17. • myocardial infarction, •cardiac dysrhythmias, • valvular heart disease, • blunt myocardial injury, • cardiomyopathy • myocardial depression- endogenous factors (e.g. bacterial and humoral agents released in sepsis) or exogenous factors CARDIOGENIC ETIOLOGY
- 18. OBSTRUCTIVE ETIOLOGY • Cardiac Tamponade •Massive Pulmonary Embolism • Tension Pneumothorax • Constrictive pericarditis
- 19. Distributive Etiology • septicshock • anaphylaxis • spinal cord injury(neurogenic shock)
- 20. ENDOCRINE ETIOLOGY • Hypo &Hyperthyroidism. • Adrenal insufficiency.
- 21. Clinical Features • Featuresof shock depend on the degree of loss of volume & on duration of shock.
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- 23. Types • Mild shock •Moderate shock • Severe shock
- 24. Mild shock • tachycardia, •tachypnoea, • mild reduction in urine output and mild anxiety. • BP is maintained though decrease in pulse pressure. • Peripheries are cool and sweaty with prolonged capillary refill times (except septic/distributive shock).
- 25. Moderate shock: • renalcompensatory mechanisms fail--urine output< 0.5 mL/kg per hour. • BP starts to fall, • drowsy and mildly confused.
- 26. Severe shock: • profoundtachycardia, • hypotension • Urine output-zero, • unconscious with laboured respiration
- 27. Stages of shock •Initial : The cells become leaky and switch to anaerobic metabolism. • Non-progressive:(compensated stage) Attempt to correct the metabolic upset of shock. loss of around 15 per cent of the circulating blood volume is within normal compensatory mechanisms • Progressive: (decompensated stage ) Eventually the compensation will begin to fail. progressive renal, respiratory and cardiovascular decompensation BP is usually maintained but falls after 30–40 per cent of circulating volume has been lost. • Refractory : Organs fail and the shock can no longer be reversed. myocardial depression and loss of responsiveness to fluid or inotropic therapy
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- 30. Monitoring • Blood pressure •Heart rate • Respiratory rate • Urine output • Blood CBC • Pulse- oximetry • ECG • U/S , CT , X-ray
- 31. Special Monitoring • CARDIO– VASCULAR - Central venous pressure Normal ; 5-10cmH2O, If CVP<5cmH2O Inadequacy of blood volume CVP>12cmH2O Cardiac dysfunction - Cardiac output Pulmonary catheter Doppler ultrasound Pulse waveform analysis
- 32. Special Monitoring • SYSTEMIC& ORGAN PERFUSION Clinical : urine output & LOC Sr. Lactate estimation & Base defecit (base deficit over 6 mmol/L-> inc morbidity) Blood gas analysis PO2 / PCO2 / ph Mixed venous O2 saturation – N – 50-70% Newer methods Muscle tissue O2 probes Near –infrared spectroscopy Sublingual capnometry
- 33. Guidelines • Treat thecause • Improve Cardiac function • Improve Tissue perfusion
- 34. Goals of Resuscitation •Overall goal: increase O2 delivery decrease demand Treatment O2 content Cardiac output Blood pressure Sedation/analgesia
- 35. Principles of Resuscitation •A: Airway patent upper airway • B: Breathing adequate ventilation and oxygenation • C: Circulation placement of adequate IV access cardiac function oxygenation
- 36. Fluid Therapy inShock • Crystalloid Solutions Normal saline Ringers Lactate solution Hartmann’s solution • Colloid Solutions • Blood transfusion Administration of inotropic or chronotropic agents to an empty heart will rapidly and permanently deplete the myocardium of oxygen stores
- 38. Oxygen Carrying Capacity •Only RBC contribute to oxygen carrying capacity (hemoglobin) • Replacement with all other solutions will support volume Improve end organ perfusion Will Not provide additional oxygen carrying capacity
- 39. Dynamic Fluid Response •Infusing 250-500ml of Fluid rapidly in 5 - 10 mts. Responders – improvement in their cardiovascular status which is sustained. Transient responders – improvement which then reverts to the previous state over the next 10–20 minutes Non – responders
- 40. Vasopressors / InotropicDrugs • Vasopressors – Phenylephrine / NA Distributive shock states Septic shock / Neurogenic administration of these agents in the absence of adequate preload rapidly leads to decreased coronary perfusion and depletion of myocardial oxygen reserves. Where the vasodilatation is resistant to catecholamines (e.g. absolute or relative steroid deficiency) vasopressin may be used as an alternative vasopressor. • Inotropics - Dobutamine Cardiogenic shock / Severe septic shock To increase the cardiac output
- 42. Other Treatments • Correctionof Acid – base balance • Steriods - Hydrocortisone • Antibiotics • Catheterisation • Nasal O2 / Ventilatory support • CVP Line • Control of Pain • ICU – Critical care management
- 43. End Points ofResuscitation Classic / Traditional • Restoration of blood pressure • Normalization of heart rate and urine output • Appropriate mental status Improved / Global • All of the above plus • Normalization of serum lactate levels • Resolution of base deficit • Adequate - MVS Goal directed approach • Urine output > 0.5 mL/kg/hr • CVP 5 -10 cm H2o • MAP 65 to 90 mmHg • Central venous oxygen concentration > 70%
- 44. Practically Speaking…. • Knowhow to distinguish different types of shock and treat accordingly. • Look for early signs of shock. • Monitor the patient using the HR, MAP, mental status, urine output. • SHOCK is not equal to hypotension. hypotension is one of the last signs of shock. patients can be in profound shock with a normal blood pressure. • • Start antibiotics within an hour ! Do not wait for cultures or blood work.
- 45. Quiz for theinterns: • 70 kg man bleeds 800ml of blood following a RTA . Classify the class of Haemorrage ? 1. I 2. II 3. III 4. IV
- 46. • Fol;owing whichcan be used to indirectly measure the base deficit: 1. Arterial pH 2. PaO2 3. Base deficit 4. Serum bicarbonate
- 47. • Death followingsevere CO poisiong is due to which type of shock: 1. Cardiogenic 2. Hypovolumic 3. Neurogenic 4. Distributive
Editor's Notes
- #3 Ambroise Paré (1510-1590), who urged the use of clysters (enemas to administer uid into the rectum) to prevent “noxious vapors from mounting to the brain.” Yet he also wrote that phlebotomy is “required in great wounds when there is fear of de exion, pain, delirium, raving, and unqui- etness”; he and others practiced bloodletting during that era because shock accompanying injury was thought to be from “toxins.” Miraculous deliverance of Anne Green, who was exe- cuted in 1650. Crile also concluded that shock was not a process of dying but rather a marshaling of the body’s defenses in patients struggling to live
- #4 Talking Points Shock is simply defined as inadequate tissue perfusion. It is also often referred to as hypoperfusion. During a shock state, inadequate amounts of oxygen and glucose are delivered to cells. In other words, the amount of oxygen delivered to the cells is less than the amount required for normal metabolism. In addition, an impaired elimination of carbon dioxide and other waste products occurs. Organs of vital importance, brain, heart, and kidneys can suffer irreversible damage, eventually leading to death. Tissue ischaemic sensitivity: - heart, brain, lung: 4-6 min.- GI tract, liver, kidney: 45-60 min.- muscle, skin: 2-3 hours
- #7 The product of anaerobic respiration is not carbon dioxide but lactic acid.
- #11 Vicious cycle
- #16 Haemorrhage control must be achieved rapidly so as to prevent the patient entering the triad of coagulopathy–acidosis– hypothermia. prolonged attempts to volume resuscitate the patient prior to surgery, which will result in further hypothermia and clotting factor dilution until the bleeding is stopped.
- #18 Forward flow of blood is inadequate bec Of pump failure due to loss of functional myocardium It is the most severe form of heart failure and it is distinguished from chronic heart failure by the presence of hypotension, hypoperfusion and the need for different therapuetic inteventions
- #19 Cardiac tamponade and constrictive pericarditis impair diastolic filling of the Rt.ventricle Tension pneumothorax limit Rt.ventricular filing by obstruction of venous return Massive pulmonary embolism increase Rt.ventricular afterload
- #20 1.characterized by loss of vascular tone SIRS: clinical response to a nonspecific insult of either infectious or noninfectious origin. SIRS is defined as 2 or more of the following variables: Fever of more than 38°C (100.4°F) or less than 36°C (96.8°F) Heart rate of more than 90 beats per minute Respiratory rate of more than 20 breaths per minute or arterial carbon dioxide tension (PaCO 2) of less than 32 mm Hg Abnormal white blood cell count (>12,000/µL or < 4,000/µL or >10% immature [band] forms) SIRS is nonspecific and can be caused by ischemia, inflammation, trauma, infection, or several insults combined. Thus, SIRS is not always related to infection. Septic shock : Gram +, Gram -/ endotoxin , Fungi / Virus, Protozoa Anaphylatic Shock:Injections - Penicillins. Anaesthetics Stings. Shelfish.
- #21 may present as a combination of hypovolaemic, cardiogenic or distributive shock. Hypothyroidism causes a shock state similar to that of neurogenic shock due to disordered vascular and cardiac responsiveness to circulating catecholamines Thyrotoxicosis may cause a high output cardiac failure. Adrenal insufficiency leads to shock due to hypovolaemia and a poor response to circulating and exogenous catecholamines.
- #28 compensated stage: the body’s cardiovascular and endocrine compensatory responses reduce flow to non-essential organs to preserve preload and flow to the lungs and brain. there is adequate compensation to maintain central blood volume and preserve flow to the kidneys, lungs and brain. Apart from a tachycardia and cool peripheries (vasoconstriction, circulating catecholamines), there may be no other clinical signs of hypovolaemia. maintained by reducing perfusion to the skin, muscle and gastrointestinal tract. systemic metabolic acidosis and activation of humoral and cellular elements within the underperfused organs. clinically occult, this state will lead to multiple organ failure and death if prolonged due to the ischaemia–reperfusion effect Decompensation Further loss of circulating volume overloads the body’s compensatory mechanisms and there is progressive renal, respiratory and cardiovascular decompensation. loss of around 15 per cent of the circulating blood volume is within normal compensatory mechanisms. Blood pressure is usually well main- tained and only falls after 30–40 per cent of circulating volume has been lost.
- #29 three stages of shock are compensatory, decompensatory, and irreversible: Compensatory shock or compensated shock, is a stage of shock in which the body is able to maintain a near normal blood pressure and perfusion of the vital organs. Decompensatory shock, decompensated shock, or progressive shock, is an advanced stage of shock in which the body’s compensatory mechanisms are no longer able to maintain a blood pressure and perfusion of the vital organs. If the shock state continues unopposed and is not managed effectively, the compensatory mechanisms become exhausted or overwhelmed, leading to a failure to maintain pressure inside the vessels and perfusion of the vital organs. Irreversible shock is the stage where, regardless of the intervention, the patient outcome is death. Cell, tissue, and organ failure and damage is so pervasive and severe that no matter what treatment is provided, organ death is inevitable and unable to be reversed.
- #32 no ‘normal’ central venous pressure (CVP) for a shocked patient, and reliance cannot be placed on an individual pressure measurement to assess volume status. Some patients may require a CVP of 5 cmH2O, whereas some may require a CVP of 15 cmH2O or higher. CVP measurements should be assessed dynamically as response to a fluid challenge. normal CVP response is a rise of 2–5 cmH2O which gradually drifts back to the original level over 10–20 minutes
- #33 The best measures of organ perfusion and the best monitor of the adequacy of shock therapy remains the urine output. level of consciousness is an important marker of cerebral perfusion, but brain perfusion is maintained until the very late stages of shock, and hence is a poor marker of adequacy of resuscitation the only clinical indicators of perfusion of the gastrointestinal tract and muscular beds are the global measures of lactic acidosis (lactate and base deficit) and the mixed venous oxygen saturation. sensitive for both diagnosis of shock and monitoring the response to therapy High mixed venous saturations (>70 per cent) are seen in sepsis and some other forms of distributive shock
- #37 Daily requirement: water: 35ml/kg/day(2.5l/day) Na: 2 mmol/kg/day K: 1 mmol/kg/day Fluid: 1 lit NS + 2 lit D5% Administration of inotropic or chronotropic agents to an empty heart will rapidly and permanently deplete the myocardium of oxygen stores and dramatically reduce diastolic filling and therefore coronary perfusion no ideal resuscitation fluid-no overt difference in response or outcome between crystalloid solu- tions (normal saline, Hartmann’s solution, Ringer’s lactate) or colloids (albumin or commercially available products). Furthermore, there is less volume benefit to the administration of colloids than had previously been thought, with only 1.3 times more crystalloid than colloid administered in blinded tria
- #41 CARDIOGENIC SHOCK The main goal is to improve myocardial function Arrhythmia should be treated Reperfusion PCI is the treatment of choice in ACS Inotropes and vasopresor