circulatory shock.pptx

circulatory shock

1. Circulatory shock Dr Thana Ram Patel Assistant professor Department of general surgery Dr SN medical college , Jodhpur

2. introduction Definition – shock = is a clinical syndrome resulting from inadequate tissue perfusion. Shock is the most common cause of death among surgical patients Shock is a systemic state of low tissue perfusion, which is inadequate for normal cellular respiration.

3. Hypovolemic shock – mc type Septic shock – hyperdynamic (early) & hypodynamic (late)

4. pathophysiology Conceptually, shock occurs at three anatomical areas of the cardiovascular system . at the heart where cardiogenic abnormalities can be either extrinsic (tension pneumothorax , hemothorax , or cardiac tamponade ) or intrinsic (myocardial infarction causing pump failure, cardiac contusion or laceration, or cardiac failure). at the large or medium vessel level in which hemorrhage and loss of blood volume leads to shock. with the small vessels in which either neurologic dysfunction or sepsis leads to vasodilatation and maldistribution of the blood volume leading to shock.

5. Severity of shock Compensated – In compensated shock there is adequate response to maintain the blood flow to kidney, lungs and brain. y Apart from tachycardia and cool peripheries there may be no other clinical signs of hypovolemia * This state is maintained by reducing perfusion to skin, muscle and GI tract. Decompensation Progressive renal, respiratory and cardiovascular decompensation results y In general loss of 15% of blood volume is compensated Blood pressure is maintained and falls after 30–40% of circulating volume has been lost

6. Complications of shock Multiple organ failure Failure of 2 or more organ systems Complication of shock Lung Acute respiratory distress Kidney Acute renal insufficiency Liver Acute liver insufficiency Clotting Coagulopathy Cardiac Cardiovascular failure

7. manifestations Sinus tachycardia, hypotension, oliguria , cold and clammy extremities, capillary refilling slow (mnemonics = shock ) Anaerobic metabolism results in metabolic acidosis due to excess lactic acid Endothelial leak is high resulting in edema Preload and after load decrease there is compensatory baroreceptor response resulting in increased sympathetic over activity- tachycardia* and vasoconstriction. Increased respiratory rate and minute ventilation to excrete excess carbon dioxide Decreased perfusion results in decreased urine output. Activation of renin angiotensin system activates, vasopressin ( antidiuretic hormone) is released leading to vasoconstriction and reabsorption of water. Cortisol is also released resulting in sodium and water reabsorption *

8. Monitoring of response Urine output (Best monitor) – urine output is best clinical guide of tissue perfusion ABG – Metabolic acidosis In shock: Only clinical indicators of perfusion of GIT and muscular beds are the measure of lactic acidosis (lactate and base deficit) and mixed venous oxygen saturation. MIXED VENOUS OXYGEN SATURATION (MVOS) The percentage saturation of oxygen returning to heart from body is a measure of oxygen delivery and extraction by tissues. Normal MVOS = 50–70% MVOS – is considered as best guide for tissue perfusion ( ie cardiac output) Local measures for perfusion: • Gastric tonometry • Gastric mucosal pH • NIR spectroscopy (Muscles) Level of consciousness ECG, oxygen saturation.

9. Types of Shock- Based on MVOS MVOS < 50% Increased oxygen consumption by cells. Cardiogenic shock and hypovolemic shock MVOS > 70% Less oxygen is delivered to cells and hence more of oxygenated blood returns. Septic shock and distributive shock*

10. CVP & PCWP Central Venous Pressure (CVP) Helps to distinguish between cardiogenic shock and hypovolemic shock CVP is not reliable indicator of left ventricular function because of the wide disparity between left and right ventricular functions Accurate therapy to monitor IV fluids, Inotropic agents and vasodilators Normal value: 0–8 mm Hg Pulmonary Capillary Wedge Pressure (PCWP)- swan Ganz pulmonary artery catheter Best Indicator for both Blood volume and Left Ventricular function than CVP Helps to differentiate: Left and right ventricular failure, pulmonary embolism, septic shock and ruptured mitral valve Measure cardiac output by thermodilution technique Normal Value: 10 mm Hg Pulmonary artery pressure: 25 mm Hg

11. Accurate method to monitor IV fluids, inotropic agents and vasodilators in shock is CVP Urine output is the Best Clinical Parameter for all kinds of shock Adequacy of resuscitation/ response is best monitored by urine output CVP is not ideal in cardiogenic shock and septic shock: In such cases pulmonary capillary wedge pressure is most sensitive Invasive arterial pressure is mandatory The best management of shock is done by putting pulmonary catheter . PCWP is considered better guide than CVP for fluid titrations as it can also determine left ventricular preload

12. Classification of shock Hypovolaemic : Hemorrhagic/ nonhemorrhagic ( Most common type of shock) Cardiogenic : Due to heart diseases Obstructive: Due to decreased preload like— tamponade , tension pneumothorax , etc. Distributive Endocrine: Hyper/Hypothyroidism and adrenal insufficiency

13. definitions Pulse rate over pulse pressure evaluation (ROPE) = pulse rate / pulse pressure = PR /(SBP-DBP) ROPE is useful in the assessment of compensated hemorrhagic shock Shock index (hemodynamic stability indicator )= heart rate / SBP Modified shock index = heart rate / mean arterial pressure (MAP) High MSI- Hypodynamic state Low MSI – hyperdynamic state

14. Treatment of shock

15. resuscitation Fluid Therapy There is no ideal fluid for resuscitation Most importantly they both have oxygen carrying capacity as zero In hemorrhagic shock the ideal fluid for replacement is blood, but for waiting time we give crystalloids. 2. Vasopressor and Inotropic Support They are not indicated as first line therapy for hypovolemic shock Drugs like phenylephrine , noradrenaline are used in distributive type of shock (sepsis or neurogenic shocks). In these cases the vasodilatation is the cause hence the drugs are beneficial. If the vasodilatation is resistant add vasopressin.

16. treatment Cardiogenic shock Noradrenaline and dopamine Hypovolemic shock Crystalloids Distributive shock Shock with oliguria Noradrenaline or phenylephrine Dopamine Anaphylactic shock Adrenaline Septic shock Broad spectrum antibiotics Hypoadrenal shock corticosteroids

17. Hemorrhagic shock The treatment for hemorrhage is arresting the bleeding and not by fluid resuscitation or blood transfusion. Primary hemorrhage: Occurring immediately as a result of an injury or surgery. Reactionary hemorrhage: It is delayed hemorrhage within 24 hours is usually caused by dislodgement of clot by resuscitation, normalization of blood pressure and vasodilation . Secondary hemorrhage: Sloughing of wall of a vessel. It usually occurs 7–14 days after injury and is precipitated by factors such as infection, pressure necrosis or malignancy. Classification Adult human has 5 liters blood (70 mL /kg in children and adults and 80 mL /kg in neonates). Hemoglobin level is a poor indicator of the degree of hemorrhage as it represents a concentration and not an absolute amount.

18. pathophysiology physiologic responses to bleeding. The advanced trauma life support (ATLS) course defines four classes of shock . In general, that categorization has helped point out the physiologic responses to hemorrhagic shock, emphasizing the identification of blood loss and guiding treatment

19. Patients often do not exhibit all of the physiologic changes described by this table, particularly those at age extremes. Due to higher water composition of their bodies, children are able to compensate with large volumes of blood loss, often exhibiting only tachycardia until they reach a tipping point where they are no longer able to compensate, at which point they have a rapid clinical decline. Elderly patients show almost an opposite physiology, as they are less equipped to compensate for blood loss and will show signs of a higher level of shock at a lower volume of blood loss. This is due to a reduced ability of cardiac compensation and fluid reserve recruitment.

20. Pulse rate increases at Class 2 hemorrhagic shock Blood pressure decreases at Class 3 hemorrhagic shock Pulse pressure decreases at Class 2 hemorrhagic shock

21. Hypothermia in shock Lethal triad of acidosis, hypothermia and coagulopathy is common in resuscitated patients who are bleeding or in shock from various factors. The optimal method to break the “vicious circle of death” is to stop the bleeding and the causes of hypothermia. Classification of hypothermia in trauma Mild: 36°C–34°C Moderate: 34°C–32°C Severe: <32°C

22. resuscitation 1. Goals of resuscitation Optimising tissue perfusion Ensuring normothermia Restoring coagulation Judicious use of crystalloids and transfusion 2. Permissive hypotension 3. Damage control surgery

23. Damage control or hemostatic resuscitation rapid control of bleeding as the highest priority; using permissive hypotension, because this would minimize the use of acellular fluids as well as potential disruption of natural clot formation; minimizing the use of crystalloid solutions. Using HTS ( Hypertonic Saline) to reduce the total volume of crystalloid necessary. Using blood products early; and considering the use of drugs, such as r FVII a or factor IX, to stop bleeding and to reduce coagulopathy

24. Balanced (traumatic ) resuscitation Trauma Resuscitation: 1:1:1 (Balanced Resuscitation) Plasma, Platelets and Packed red blood cells in a 1 : 1 : 1*** When red blood cells are transfused match each unit with one unit of platelets and 1 unit FFP ( 1:1:1). This balanced approach will not correct coagulopathy although it can prevent coagulopathy happening. Correct underlying coagulopathy should be treated.

25. Recent advances Massive resuscitation: Most patients do not require massive transfusion, usually defined as a transfusion of more than 10 units of PRBCs in 24 hours** Recent Advances in Resuscitation: Allowing permissive hypotension Minimizing crystalloid resuscitation Using HTS, Aggressively using blood and blood products

26. Distributive (septic) Shock Includes anaphylactic shock, septic shock and spinal cord injury ( neurogenic shock) Inadequate organ perfusion is associated with vascular dilatation and hypotension, low systemic vascular resistance, inadequate afterload and a resulting abnormally high cardiac output In anaphylaxis vasodilatation is due to excess histamine release

27. Septic shock( vasodilatory shock) Causes of Vasodilatory Shock Systemic response to infection Noninfectious systemic inflammation: Pancreatitis, Burns Anaphylaxis Acute adrenal insufficiency Prolonged severe hypotension: Hemorrhagic and cardiogenic shock Metabolic: Lactic acidosis, carbon monoxide poisoning Terms in Sepsis Sepsis: Evidence of infection + systemic signs of inflammation Severe sepsis: Hypoperfusion with signs of organ dysfunction Septic shock: Presence of above with more significant evidence of tissue hypoperfusion and systemic hypotension

28. SIRS n septic shock definitions SIRS Two or more of the following: • Temperature >38°C or <35°C Heart rate >90 beats/min Respiratory rate >20 breaths/min or PaCO2 <32mmHg WBC count >12,000 or4,000 Sepsis= SIRS + documented infection Severe Sepsis= Sepsis + one or more organ dysfunction or hypoperfusion (e.g., Iacticacidosis , oliguria , altered mental status) Septic Shock= Sepsis + organ dysfunction + hypotension (SBP 90 mm Hg with vasopressors )

29. Systemic inflammatory response syndrome( SIRS) It is final common pathway in shock of any cause where there is failure of inflammatory localization with vasodilation , increased endothelial damage, thrombosis, leucocyte migration and activation It is a part of severely decompensated reversible shock which eventually leads to multiple organ dysfunction syndrome (MODS), irreversible shock wherein patient is anuric , drowsy, cold and terminally ill. SIRS carries poor prognosis

30. treatment Airway, breathing and circulation Hypotension is managed with Fluids* Balanced salt solution Next antibiotics are given to take care of sepsis Vasopressors : Like dopamine, dobutamine , epinephrine form second-line therapy