Pathophysiology of shock,Mitral Re,AMI Late Complicationgurgitation

Circulatory shock is a process in which blood flow and oxygen delivery to tissues are disturbed
Leads to tissue hypoxia –compromise of cellular metabolic activity and organ dysfunction
Shock results from four potentials pathophysiological mechanisms
Hypovolemia
Cardiogenic factors
Obstruction
Distributive factors
Right ventricular Infarct

1. Hypotension & shock Dr Shine Linn Aung Supervised By Dr Yin Min Thu Zar

2. Outlines Pathophysiology of shock Types of shock Focused assessment Management outlines 4/28/2024 hyotension and shock 2

3. Pathophysiology of shock Circulatory shock is a process in which blood flow and oxygen delivery to tissues are disturbed Leads to tissue hypoxia –compromise of cellular metabolic activity and organ dysfunction Shock results from four potentials pathophysiological mechanisms Hypovolemia Cardiogenic factors Obstruction Distributive factors 4/28/2024 hyotension and shock 3

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6. Types of shock Most common cause

7. 4/28/2024 hyotension and shock 7 Right ventricular Infarct Due to RCA occlusion RCA supply blood to SA node, AV node, RV, LV-posterior and inferior Associated with arrhythmia, inferior AMI, Posterior AMI Inferior MI + Shock Complete heart block RV infarct Treatment IV fluid resuscitation f/b inotropes (individualized) PCI/Thrombolysis C.I – Vasodilator (Morphine, Nitrate ), Diuretics

8. 4/28/2024 hyotension and shock 8 Aortic Stenosis Precordial examination I&P - apex is not displaced, heaving in character, double apical pulsation A – NL S1, ESM, Ejection click, Soft S2(Single S2/Reverse S2) radiating to carotid, S4

9. 4/28/2024 hyotension and shock 9 Mitral Regurgitation Backward flow problem Pulse, BP, JVP – NL Precordial examination I&P – LVH features (apex beat displaced, heaving), RVH features (Epigastric pulsation, LPH) A – Soft S1, PSM, NL S2, S3/MDM (due to volume overload)

10. 4/28/2024 hyotension and shock 10 AMI Late Complication Myocardium – Cardiac rupture syndrome VSD MR Free wall rupture VSD – RVF +/- LVF (Acute Pulmonary Edema + Shock), PSM loudest at tricuspid area MR – MR features, Associated with Inferior MI, PSM loudest at apex and radiate to left axilla Free wall rupture – Cardiac tamponade (pericardial effusion + shock)

11. 4/28/2024 hyotension and shock 11 Adrenal insufficiency Suspect adrenal insufficiency if features of glucocorticoid insufficiency presence Unexplained shock (especially in case of malignancy, sepsis, Cushingnoid appearance/long-term steroid use) Unexplained postural hypotension Unexplained arthralgia and myalgia Unexplained GI symptoms (especially if vomiting, Hyperkalemia) Investigation Baseline – Hyponatremia , Hypoglycemia , Hyperkalemia, Ca2+ ACTH stimulation test – Short Synacthen test Localization test – ACTH level, 21-hydroxylase adrenal Autoantibodies, Pituitary hormones

12. Focused assessment Assessment using ABCDE method 8 key questions to ask yourself Is there obvious hemorrhage from GI tract or other site(AAA)? Is there a major arrhythmia? Is there ECG evidence of ACS ( ST elevation or depression , new left bundle branch block)? Is there associated pulmonary oedema , indicating cardiogenic shock? 4/28/2024 hyotension and shock 12 STEMI Equivalent

13. 5.Is there fever or other features pointing to sepsis? 6.Is there pulmonary embolism? 7..Is there tension pneumothorax? 8.Could this be anaphylaxis? 4/28/2024 hyotension and shock 13

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16. Management outlines Keypoint – make a diagnosis and give a specific management V-ventilate(oxygen administration) I-infuse( fluid resuscitation) P-Pump (administration of vasoactive agents) 4/28/2024 hyotension and shock 16

17. Ventilatory support Administration of oxygen should be started immediately to increase oxygen delivery and prevent pulmonary hypertension Invasive ventilation – patients with severe dyspnoea , hypoxia, persistent or worsening acidemia ( ph <7.3) Target-Pa O2>8 Kpa, arterial saturation>90% 4/28/2024 hyotension and shock 17

18. Fluid resuscitation Fluid therapy to improve microvascular blood flow and increase cardiac output is an essential part of the treatment of any form of shock. Fluids of choice = crystalloid solution( Ringer lactate / 0.9% Normal Saline) If there is no pulmonary oedema -give IV crystalloid 500 ml over 15 min –reassess clinical responses Determination of fluid responsiveness-check changes in clinical parameters (arterial BP , urine output, cardiac filling pressures) 4/28/2024 hyotension and shock 18

19. Hypovolemic shock Result from a decreases in effective intravascular volume - decrease venous return to right ventricle Aim- reestablishing the adequacy of the intravascular volume Rapidly transfuse crystalloid 500 ml to 1 liter until SBP around 100 mmHg Blood products should be transfused to patients with significant anemia or active hemorrhage. Target Hb - 80 g/l Young patients- tolerate HCT of 20% to 25% Older patients - >30 % of HCT to optimize oxygen delivery to tissues 4/28/2024 hyotension and shock 19

20. Major hemorrhage 50% of blood volume loss within 3 hours ( eg , 2500ml for 70 kg adult) Blood loss of 150ml/min HR>120 min , SBP <90mmhg indicate occult bleeding Bleeding –goals Find the bleeding, stop bleeding Rapid restoration of effective blood volume Maintain haemostasias , oxygen carrying capacity 4/28/2024 hyotension and shock 20

21. Correct clotting abnormalities PT >1.5× control - give iv vitamin K 10 mg and 2 units of FFP Plt count<75×10 12 /l - give platelet concentrate Fibrinogen<1.5 g/l, give cryoprecipitate Consider tranexamic acid - 1G over 10 min f/b infusion of 1 G over 8 hrs 4/28/2024 hyotension and shock 21

22. 4/28/2024 hyotension and shock 22 Hypovolemic shock RRR R esuscitation R eplacement of the loss R emoval of the cause

23. Cardiogenic shock Result of pump failure - hypotension (MAP <60 mmHg),decreased cardiac index (<2 l/min/m2), elevated intracardiac pressures, increased peripheral vascular resistance and organ hypoperfusion. Careful attention to fluid management – to ensure adequate preload( especially in RV infarction ) and to avoid acute pulmonary oedema. Definitive treatment - angioplasty (PCI or thrombolysis) Correct arrhythmia - DC cardioversion or IV Amiodarone or digoxin infusion 4/28/2024 hyotension and shock 23

24. Obstructive shock The commonest Cause- Massive pulmonary embolism Goals - to preserve peripheral organ perfusion and removing vascular obstruction Fluid administration and use of vasopressors Definitive Tx-thrombolytic therapy or surgical embolectomy 4/28/2024 hyotension and shock 24

25. Distributive shock Two forms associated with significant vascular tones= septic shock & anaphylactic shock Septic shock- caused by the systemic release of mediators that is usually triggered by circulating bacteria or their products- hypotension due to decreased vascular tone Main goals- initial fluid resuscitation, adequate treatment of underlying infection and interruption of the mediator-associated systemic inflammatory response. 4/28/2024 hyotension and shock 25

26. Fluid administration and vasoactive agents Goals- to achieve MAP> 65 mmHg, CVP> 8 mmHg and central venous blood oxygen saturation >70% Initial bolus fluid- 500ml or 1 L crystalloid Refractory hypotension to fluid therapy = Vasoactive agents - Noradrenaline or Dopamine Systemic low dose corticosteroid for relative adrenal insufficiency Empirical Antibiotics therapy 4/28/2024 hyotension and shock 26

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28. 4/28/2024 hyotension and shock 28 Sepsis Six 3 In, 3 Out 3 In – Antibiotics, Fluid, Oxygen 3 Out – Blood culture, Lactate, U.O

29. Anaphylactic shock Remove the trigger IM 0.5 mg of Adrenaline on anterolateral aspect of the thigh Repeat 5 minutes if no improvement Monitor HR,BP, O2 saturation Fluid -500 ml to 1L of crystalloid If wheeze- Nebulized bronchodilator ( eg , salbutamol) If no improvement after 2 doses of IM adrenaline- get expert help 4/28/2024 hyotension and shock 29

30. Vasoactive agents TWO types- Vasopressors - Noradrenaline, Dopamine Inotropic agents - dobutamine , phosphodiesterase type III inhibitors-milrinone , enoximone, levosimendan 4/28/2024 hyotension and shock 30

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32. References Oxford handbook of clinical medicine 11 th edition Acute medicine 5 th edition Washington manual of medical therapeutics 34 th edition Pathophysiology of disease 8 th edition Circulatory shock : NEJM Review article 4/28/2024 hyotension and shock 33

33. 4/28/2024 hyotension and shock 34 Thank you for paying attention