Shock

hypovolemic, cardiogenic, anaphylactic, obstructive and hypoadrenal shock syndromes

1. SHOCK CLASSIFICATION, PATHOPHYSIOLOGY, MANAGEMENT Dr. POOJA M. N. Assistant Professor Dr. KSHAMA BALAKRISHNA Post Graduate

2. What is Shock? SAMUEL V GROSS, 1872 said - “ Shock is the manifestation of the rude unhinging of the machinery of life ” Shock is a state of acute circulatory insufficiency that creates an imbalance between tissue oxygen supply (delivery) and oxygen demand (consumption) resulting in end-organ dysfunction A clinical syndrome that results from inadequate tissue perfusion Failure of circulation centrally or peripherally to meet the metabolic demands of the tissues A group of life-threatening circulatory syndromes with varying physiological profiles.

3. CLASSIFICATION Hypovolemic Shock or Haemorrhagic Shock Cardiogenic Shock Obstructive Shock or Cardiac Compressive Shock Vasogenic or Distributive Shock Septic Shock Anaphylactic Shock Neurogenic Shock

4. HYPOVOLEMIC SHOCK A decrease in circulating volume in relation to the total vascular capacity and characterized by a reduction of diastolic filling pressures resulting in poor tissue perfusion. Commonest cause being trauma resulting in external or concealed haemorrhage from blunt or penetrating injuries.

5. ETIOLOGY Hemorrhagic shock - severe blood loss leads to inadequate oxygen delivery at the cellular level. Traumatic Blunt or penetrating injury Fractures- long bones, pelvic fractures Non- Traumatic GI bleeds Aortic dissection Rupture of large vessel aneurysm Erosion of a large vessel Diffuse inflammation of mucosal surfaces

6. Due to loss of water and electrolytes, with fall in effective circulating volume. Traumatic Burns Crush injuries Non-traumatic Fluid loss from vomiting or diarrhoea ( eg - cholera) Fluid loss in diabetes mellitus, adrenal insufficiency, excessive sweating, diabetes insipidus Fluid sequestration ( eg - intestinal obstruction, pancreatitis) ETIOLOGY

7. PATHOPHYSIOLOGY Ventricular preload - DBP and volume Decreased SV and CO, hence SBP CO leads to SVR to maintain perfusion to heart and brain at the expense of other tissues ( muscle, skin, gut) Autoregulation occurs at heart and brain- maintenance of blood flow over wide range of perfusion pressure (60- 150mm of Hg).

8. Neurohumoral Compensatory Mechanisms - Catecholamines Cortisol ADH secretion RAS activation Shift of fluid from extravascular compartment to vascular compartment PHASE 1- <1 hr of blood loss, shift from interstitium to capillaries (may continue upto 40hrs) PHASE 2- RAS activation- Na + and water retention to replenish interstitial fluid PHASE 3- Erythropoesis . PATHOPHYSIOLOGY

9. DETERMINANTS Arterial oxygen content CaO 2 = (1.39 x Hb x SaO 2 ) + (PaO 2 x 0.0031) Oxygen delivery= Cardiac Output x Arterial O 2 content DO 2 = CO x [ (1.39 x Hb x SaO 2 ) + (PaO 2 x 0.0031 )] Oxygen consumption= Cardiac Output x (Arterial O 2 content- Venous O 2 content) Vo 2 = CO x (CaO 2 - CvO 2 ) = CO x Hb x 1.39 ( SaO 2 - SmvO 2 )

10. MICROVASCULATURE Impairment of microcirculation- central pathophysiology of shock Imbalance between vasoconstrictors ( Angiotensin II, endothelin-1, thromboxane A 2 ) and vasodilators (PGI 2 , NO, adenosine) CELLULAR RESPONSE

11. ORGAN RESPONSE Endocrine Increased gluconeogenesis and lipolysis . In critically ill, cortisol levels and ACTH stimulation is decreased, hence survival rates are low. Pancreas- increased secretion of glucagon- increased gluconeogenesis increasing blood glucose levels. Renal Response Decreased urine output Hypoperfusion – AKI Acute tubular necrosis

12. ORGAN RESPONSE Cardiovascular response Hypovolemia preload SV HR CO(limited) Venoconstriction Shock induced decreased myocardial filling causes decrease in LV end-diastolic volume and fall in SV Hypothermia, myocardial ischemia and acedemia impairs myocardial contractility and SV. Shock Index, SI= HR/SBP (normal= 0.5-0.7)

13. Pulmonary Response ORGAN RESPONSE

14. HAEMORRHAGIC SHOCK Definition of Massive Haemorrhage Loss of more than one volume of blood in 24hrs 50% total blood volume lost in 3hrs Bleeding in excess of 150mL/min Lethal Triad

15. How does a patient present? Clinical Features: Pallor Slight anxiety/ restlessness Cold, clammy skin Tachycardia Collapsed neck veins Oliguria (<0.5ml/kg/hr) or anuria “Any patient who is cool and tachycardic is in shock until proven otherwise”(ATLS)

16. STAGES

17. Factors STAGE I STAGE II STAGE III STAGE IV Blood loss (mL) 750 750-1500 1500-2000 2000 or more Blood loss (% blood volume) 15 15-30 30-40 40 or more Pulse (beats/min) <100 >100 >120 140 or higher Blood pressure Normal Orthostatic Decreased Decreased Pulse pressure (mm Hg) Normal or increased Decreased Decreased Decreased Capillary refill test Normal Positive Positive Positive Respirations per minute 14-20 20-30 30-40 >40 Urine output (mL/hr) 30 20-30 <20 Negligible CNS: mental status normal anxious Anxious, confused Confused, lethargic Fluid replacement Crystalloid Crystalloid Crystalloid + blood Crystalloid + blood Baskett’s Classification of Haemorrhagic Shock

18. Vitals (PR, BP, RR, temp) Urine output, capillary refill time, JVP, ABG Hematocrit Classic hemodynamic pattern- low CVP, low PCWP, low CO and high SVR. Oxygen extraction ETCO2 SaO2 SvO2 O2 extraction (SaO2-SvO2) Normal >95% 65-70% ~30% Hypovolemic >95% 50-65% 30-50% Shock >95% <50% >50% Monitoring a case of hypovolemic shock

19. Bedside USG- assess right-sided filling pressures, IVC diameter and caval index The Rapid Ultrasound in Shock ( RUSH) exam involves a threepart bedside physiologic assessment simplified as the pump (cardiac), the tank (volume status ) and the pipes (arterial and venous)

20. MANAGEMENT Fluid Resuscitation- Restoring volume is the keystone VO2= CO x Hb x 1.39 x (SaO2- SvO2) Fluid challenge- 500 or 1000mL NS rapidly infused over 20min and reassess the patient after each bolus Cannulation Site Catheter Dimensions and relation to flow rate Infusion Device Length (inches) Flow rate (mL/min) Peripheral 14G catheter 2 195 16G catheter 2 150 Central 16G catheter 5.5 91 16G catheter 12 54

21. Relation to fluid viscosity and flow rate Estimating volume requirement Male 65ml/kg ; Female 60ml/kg Volume is replaced by calculating the volume deficit crystalloids in 3:1 ratio and colloids and blood at 1:1 ratio Fluid Flow rate (mL/min)* Crystalloids 100 5% albumin 100 Whole blood 65 Packed cells 20

22. VASOPRESSOR SUPPORT

23. MASSIVE TRANSFUSION PROTOCOL STEP 1- CONTROL BLEEDING Minimise time between arrival and surgery if indicated – “Damage Control Surgery” Use of tourniquet , tamponade techniques, drugs STEP 2- IDENTIFY THE NEED FOR MASSIVE TRANSFUSION ABC score (4points) TASH score (6points) Identify massive trauma / bleed on purely clinical basis Based on volume requirements after an initial resuscitation.

24. STEP 3- ACTIVATE HOSPITAL MASSIVE TRANSFUSION SYSTEM STEP 4-INITIAL EMPIRICAL RESUSCITATION (1 ST 15 – 30 MIN) FBP, cross match, coagulation profile (INR, APTT, fibrinogen), ABG (VBG) Uncrossmatched (O Rh -) PCV– 2 units. FFP (ABO specific)– 2 bags. (1:1 ratio) STEP 5- CONTINUE VOLUME RESUSCITATION /MONITORING Target MAP 65-70mm of Hg ; 90-100 in head injury/ raised ICP Reassess

25. STEP 6: CONSIDER OTHER AGENTS FOR PREVENTION / LIMITATION OF COAGULOPATHY Obstetric haemorrhage: early use of cryoprecipitate is recommended. Platelets: only recommended in thrombocytopenia < 50,000. Tranexamic acid: give 1 g loading dose (over 10 mins ) STEP 7:TARGET THERAPY TO RESULTS if Hb < 8g/ dL - PCV ; if INR > 1.5 or APPT > 50 sec- 2U FFP; if fibrinogen < 1.0 g/ dL - 8U of CP Calcium is < 1.1mmol then, 1 amp of Calcium gluconate 1g/10ml Maintain temperature > 35 degrees STEP 8: EVACUATION PLANNING

26. ENDPOINTS ABG- pH, lactate, bicarbonate, SaO2 Vital Parameters- PR, BP, U/O=>0.5mL/kg/ hr MAP>65mm Hg, CVP- 8-12mm Hg, ScvO2>70% Bedside Echo- assess intravascular volume and cardiac function IVC diameter 1.5-2.5cm. Trauma<1cm, <1.5cm volume depletion, >2.5cm overload Caval index- ( IVC exp -IVC insp ) diameter/IVC exp *100, volume deletion <50%, >50% fluid responsivesness Achievement to baseline with in 24hrs-markedly improved survival rate

27. CASE SCENARIO A 20yr old female, C/O primigravida , with h/o ammenorrhoea of 22 weeks with severe abdominal pain. Patient had tachycardia with low BP, with severe generalised pallor. UPT+, B- Hcg +. USG abdomen revealed normal ovaries, no gestational sac seen in the uterus with moderate to severe fluid collection seen in abdomen and pelvis. Patients was immediately taken up for emergency exploratory laparotomy for suspected ruptured ectopic pregnancy with hemoperitoneum . On PAC, patient was in obvious distress . PR-130bpm, regular in rhythm, of low volume, BP-86/66 mmHg in supine position with severe pallor. A irway examination she had adequate mouth opening Pre-op tests- Hb-2.7g/ dL , TC-25300 cells/ cumm , plt-2.96 lakhs/ cumm and PT and INR were normal

28. Anaesthetic management Plan of anaesthesia- GA Informed consent - risk of bleeding, multiple blood transfusions, general anaesthesia related complications Two wide bore 16 or 18G IV lines. Standard monitors- PR, BP, SpO2, ECG Invasive monitors like CVP line & arterial line Premed - Inj Ranitidine 50mg, Ing Metaclopromide 10mg, Inj. Glycopyrolate 0.2 mg and Inj Fentanyl 2mcg/kg. RSI with Inj Ketamine 1-2mg/kg and Inj Succinylcholine 2mg/kg Maintenance- Isoflurane and intermittent boluses of fentanyl. NDMB- Atracurium 0.5mg/kg Fluid resuscitation- RL, Colloids, NS; use of fluid warmer to avoid hypothermia; Vasopressors Blood components- PRBC, FFP at 1:1 ratio; Inj. Calcium gluconate Intra-op ABG- correction accordingly Watch endpoints ; Prolonged surgery- ICU with post op monitoring

29. CARDIOGENIC SHOCK “ Cardiogenic shock (CS) is a low-cardiac-output state resulting in life-threatening end-organ hypoperfusion and hypoxia” Cardiogenic shock is defined as sustained hypotension with tissue hypoperfusion in spite of adequate left ventricular filling pressure.

30. CLINICAL CRITERIA

31. EPIDEMIOLOGY Incidence of cardiogenic shock after an acute MI varies from 5-19% In 60% patients, shock develops <48hrs and in about 30% it occurred >4days after MI. It carries mortality of over 80%. LV failure accounts for ~80% cases of cardiogenic shock complicating acute MI. Acute severe MR, ventricular septal rupture, predominant RV failure, free wall rupture or tamponade account for the remainder.

32. ETIOLOGY

33. Risk Factors For Cardiogenic Shock Complicating Acute MI

34. PATHOPHYSIOLOGY

35. HEMODYNAMIC PHENOTYPES

36. Patients at risk of cardiogenic shock following MI Proximal obstruction of just LAD artery- infarction of >40% of LV wall Patients with critical three vessel disease Acute massive LV infarction Inferior wall MI, when it involves RV Non- functioning myocardium > critical level (35%)

37. Factors that may trigger or potentiate shock in acute MI Hypovolemia Tachy/ brady -arrhythmias Depressant action of drugs- use of propranolol in early or insidious pump failure, oversedation with narcotics may induce hypotension Metabolic acidosis, dyselectrolytemia Unrelieved pain Unrelieved hypoxia Pulmonary embolism

38. Refractory chronic heart failure Reasons why chronic heart failure may decompensate with cardiogenic shock Development of new comorbid condition Progression of underlying disease Infection/sepsis Myocardial ischemia Renal insufficiency Chronic renal insufficiency Uncontrolled diabetes Uncontrolled HTN Anemia Pulmonary embolism Poor patient compliance with drug therapy Hypo/hyperthyroidism

39. CLINICAL FEATURES Chest pain, dyspnoea Cold, pale, clammy, diaphoretic peripheries Rapid thready pulse SBP<90mm of Hg, MAP<55mm of Hg Urine output< 35ml/ hr with Na + <30mEq/L Impaired cerebration Cheyne -Stokes respiration Weak apical impulse, soft S 1 , S 3 gallor + Acute MR, VSR – systolic murmur LV Failure Chest rales B/L pedal edema RV Failure Jugular venous distension Positive Hepatojugular reflex

40. Laboratory finding CBC, cardiac markers, RFT, LFT, ABG ECG Chest X-Ray Echo – severity of MR, left to right shunt in case of VSR, evidence of pulmonary embolism PAC catherization - measurement of filling pressures and CO LV catherization and coronary angiography DIAGNOSIS

41. MANAGEMENT Principles Improve CO and tissue perfusion Reduce or relieve severe pulmonary edema Maintain a clear airway and a PaO 2 of atleast 70mm Hg Correction of electrolyte and acid-base balance Recognize and treat factors which potentiate or aggravate shock Improve hemodynamic profile

42. Definitive management Augment cardiac output by one of three ways: Pharmacological inotropic support Revascularisation with: Thrombolysis Percutaneous intervention Coronary artery bypass surgery Intra-aortic balloon counterpulsation

43. Circulation. 2017;136:e232–e268. DOI:10.1161/CIR.0000000000000525

44. Treating Pulmonary Edema Patients with acute cardiogenic pulmonary edema generally have an identifiable cause of acute LV failure—such as arrhythmia, ischemia/infarction , or myocardial decompensation SUPPORT OF OXYGENATION AND VENTILATION Oxygen Therapy - goal is SpO2 ≥92% Positive pressure ventilation- reduces work of breathing, improves oxygenation. Mechanical ventilation- benefits of using PEEP D ecreases both preload and afterload Redistributes lung water from the intraalveolar to the extraalveolar space Increases lung volume to avoid atelectasis.

45. Renal Replacement Therapy- Continuous renal replacement therapy preferred, especially in patients with hypotension or inotropic support REDUCTION OF PRELOAD Diuretics- furosemide at ≤ 0.5 mg/kg Nitrates - NTG and isosorbide dinitrate . Sublingual NTG (0.4 mg × 3 every 5 min) is first-line therapy for acute cardiogenic pulmonary edema . If pulmonary edema persists in the absence of hypotension, it may be followed by IV NTG, starting at 5–10 μg /min Morphine - 2- 4mg IV boluses ACE inhibitors- reduce myocardial remodelling Other agents- Nestritide , Digitalis Glycosides

46. Anaesthetic considerations Goals Avoid cardiac depressive drugs ( eg - Propofol , Halothane) Maintain normovolemia Avoid increase in afterload Use of inotropic drugs if required Emergency antiarrhythmic drugs within reach Adequate analgesia

47. Anaesthetic considerations Detailed history and examination Informed and written high risk consent Judicious titration of drugs and fluids in patients with low ejection fraction Appropriate premedication Etomidate - Induction agent of choice NMDR- Vecuronium Post-op ICU care

48. OBSTRUCTIVE SHOCK Obstructive shock or cardiac compressive shock is a low output state with inadequate perfusion resulting from compression of the heart and great veins opening into the right heart causing sharp reduce in diastolic filling. High intrathoracic pressures- causing compression of the large veins opening into the right heart and heart chambers .

49. ETIOLOGY Impaired Diastolic filling (reduced ventricular preload) Direct venous obstruction (vena cava) Increased intrathoracic pressure Decreased cardiac compliance Impaired Systolic contraction Acute pulmonary hypertension Massive pulmonary embolism Aortic dissection

50. CLINICAL FEATURES Signs of poor peripheral perfusion Distended neck veins Tension pneumothorax E levated intrapleural pressure collapses intrathoracic great veins which leads to inadequate venous filling H yperresonant chest,absent breath sounds on affected site,mediastinum shifted to opposite side Displacement of trachea with distended neck veins- pathognomic sign of tension pneumothorax

51. Cardiac Tamponade

52. TREATMENT Treatment of choice for cardiac tamponade is pericardial drainage Tension Pneumothorax- Intercostal chest tube drain at second ICS . Pulmonary embolism is usually treated with systemic anticoagulation, but when massive pulmonary embolism causes right ventricular failure and shock, thrombolytic therapy should be strongly considered.

53. SEPTIC SHOCK “Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection.” Sepsis is a syndrome of physiological, pathological, and biochemical abnormalities induced by infection. Septic shock defined as a subset of sepsis in which profound circulatory, cellular and metabolic abnormalities are associated with a greater risk of mortality than with sepsis alone.

54. TERMINOLOGY Bacteremia : transient invasion of circulation by bacteria Septicemia : prolonged presence of bacteria in the blood accompanied by systemic reaction SIRS (systemic inflammatory response syndrome ): it is a syndrome characterized by the presence of two or more of the following clinical criteria:  Temperature(core) >38°C HR>90beats/min Respiratory rate >20b/min or PaC02 <32 mmHg WBC>12000/mm 3 or <4000/mm 3 or >10% immature bands .

55. When sepsis is accompanied by hypotension that is refractory to volume infusion, the condition is called Septic shock. Early stages Hyperdynamic or “warm” shock Late stages Hypodynamic or “cold” shock Criteria Sepsis- Sequential (sepsis-related) Organ Failure Assessment (SOFA) score ≥2 above baseline values Septic shock - vasopressor requirement to maintain a MAP≥ 65 mmHg and a S.lactate >2 mmol /L in the absence of hypovolaemia

56. SOFA SCORE

57. NEUROGENIC SHOCK Neurogenic shock is the interruption of autonomic pathways leading to hypotension and bradycardia (and hypothermia). It is common in injuries involving cardiac sympathetics (T2 –5) resulting in a decrease in systemic vascular resistance, decreased inotropism , and increased unopposed resting vagal tone. CAUSES High cervical spinal cord injury (vertebral body #) Inadvertent cephalad migration of spinal anaesthesia Epidural hematoma or devastating head injury

58. PATHOPHYSIOLOGY Initial- massive release of catecholamines - HR, BP Followed by, fall in sympathetic tone- BP When T2-T5 involved- vasodilation , inotropism , HR

59. PATHOPHYSIOLOGY Loss of reflexes below the level of spinal cord injury C/F- flaccid areflexia , hypotension Gradual return of reflex activity when the reflex arcs below redevelop This is a complex process and a recent four-phase classification to spinal shock has been postulated: Areflexia (Days 0– 1) Initial reflex return (Days 1–3) Early hyperreflexia (Days 4–28) Late hyperreflexia (1–12 months).

60. CLINICAL FEATURES Alert and responsive-if head injuries are absent Warm extremities above level of injury Cool -below level of injury Diaphragmatic breathing Hypotension without obvious cause Bradycardia Priapism Flaccid areflexia (e.g. in legs but tone in arms) Loss of pain response below a level.

61. TREATMENT Fluid resuscitation- with NS Vasopressor support Early vasopressor support has been advocated to ensure adequate spinal cord perfusion pressure and reduce secondary cord injury. Supportive measures Surgery Stabilization, open or closed reduction, and surgical decompression must be considered to relieve direct pressure on the cord and prevent secondary injury

62. ANAPHYLACTIC SHOCK ‘‘a serious, generalized or systemic, allergic or hypersensitivity reaction that can be life-threatening or fatal’’   Ana- phylaxis means– (anti)- phylaxis , protection or guarding. Anaphylaxis is a potentially life-threatening systemic allergic reaction involving one or more organ systems occuring within seconds to minutes of exposure to the anaphylactic trigger.

63. ANAPHYLACTIC SHOCK Anaphylactic shock is an anamnestic response of an individual to an antigen which is characterized by Severe vasodilation Bronchoconstriction Pruritis Increased vascular permeability

64. ETIOLOGY Drugs Blood products and vaccines Diagnostic agents Venom Hormones Extracts of allergens used for desensitization Food

65. PATHOPHYSIOLOGY EFFECTOR MOLECULES AND RECEPTORS IgE mediated (with prior sensitization) Non- IgE mediated reactions Role of IgG and FcgRs Role of complement

66. POTENTIAL EFFECTOR CELLS OF ANAPHYLAXIS Mast cells – key cells Basophils Neutrophils Monocytes and macrophages Histamine Platelets PAF CystLTs Other mediators include prostaglandins, TNF-α POTENTIAL MEDIATORS OF ANAPHYLAXIS

67. DIAGNOSIS History Signs and symptoms Identify the specific cause Serum biomarker – Histamine Useful biomarker - S.tryptase

68. TREATMENT Early recognition First line – A B C Patient position- upright or sitting posture may lead to the “empty heart syndrome” Second line- used to treat anaphylaxis refractory to the first-line treatments or associated with complications

69. Drugs In Daily Anaesthetic Practice With Risk Of Anaphylaxis Local Anaesthetic- Lignocaine (preservative – methyl paraben ) Muscle relaxants- Atracurium , rocuronium IV induction agents- Propofol , Etomidate (egg lecithin based) Narcotics- Morphine Analgesics- NSAIDS Dextrans Latex exposure

70. HYPOADRENAL SHOCK Unrecognized adrenal insufficiency complicates the host response to the stress induced by acute illness or major surgery. Etiology Chronic administration of high dose of corticosteroids Relative hypoadrenal state Idiopathic atrophy- Etomidate induction Tuberculosis Metastatic disease B/L adrenal haemorrhage Amyloidosis

71. Clinical features: Loss of homeostasis- reduction in SVR, hypovolemia , reduced CO. Management: ACTH stimulation test for diagnosis- may or may not be consistent Treatment Dexona 4mg - persistently hemodynamically unstable patients. Dexona can be started empirically Hydrocortisone 100mg Q6hrly or Q8hrly Volume resuscitation and inotropic support

72. CONCLUSION As Anaesthesiologists and Intensivists, it is important to understand the pathophysiology, recognise a patient in shock and prompt treatment. Rapid assessment with resuscitation Source control ( Bleeding, Infection) – Highest priority Regardless of source, the fundamental primary treatment of shock remains recognition & stabilisation of hemodynamics . In trauma Arrival to on table time – very crucial Practicing in a developing country, and in a tertiary care hospital, we must be skillful in using minimal resources to give the best possible outcome.

73. REFERENCES Principles of Critical Care, Udwadia , 2 nd edition The ICU Book, Paul Marino, 4 th edition Harisson’s Principles of Internal Medicine, 20 th edition Tintinalli’s Emergency Medicine, A Comprehensive Study Guide, 8th edition Goldmann and Cecil, Textbook of Medicine, 25 th edition N Engl J Med 2018;378:370-379 DOI:10.1056/NEJMra1705649 Circulation. 2017;136:e232–e268. DOI:10.1161/CIR.0000000000000525 frca.uk.co Continuing Education in Anaesthesia, Critical Care & Pain | Volume 13 Number 6 2013 doi:10.1093/ bjaceaccp /mkt021 American Academy of Allergy, Asthma & Immunology http://dx.doi.org/10.1016/j.jaci.2017.06.003 Ms Sharene Pascoe, Ms Joan Lynch 2007, Adult Trauma Clinical Practice Guidelines, Management of Hypovolaemic Shock in the Trauma Patient ,NSW Institute of Trauma and Injury Management.