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Circulatory failure in Intensive Care

Circulatory failure in Intensive Care. Dr…. Circulatory System. Ensures adequate blood flow to supply metabolic demands of the tissues Regulation via cardiac pump and peripheral vascular system Pump control varies the cardiac output

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Circulatory failure in Intensive Care

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  1. Circulatory failure in Intensive Care Dr….

  2. Circulatory System • Ensures adequate blood flow to supply metabolic demands of the tissues • Regulation via cardiac pump and peripheral vascular system • Pump control varies the cardiac output • PVS control regulates intravascular volume, vascular resistance, perfusion pressure and appropriately distributes flows to vascular beds

  3. Circulatory failure = shock ‘Tissue perfusion is inadequate for the metabolic needs of the patient’

  4. Inadequate O2 delivery • Inadequate O2 delivery represents an imbalance of delivery relative to need • This imbalance between supply and demand leads to the development of tissue hypoxia • Changes in systemic perfusion are always present in shock

  5. Classification of Shock • Cardiogenic • Infarction/ischaemic VSD/myocarditis • Valvular abnormalities/PE/Tamponade • Hypovolaemic • Haemorrhage • Excessive fluid loss from GI/Renal tracts/Burns • Septic • Neurogenic • Anaphylactic

  6. Oxygen delivery (DO2) • Amount of O2 delivered to peripheral tissues • Dependent on arterial O2 content and cardiac output • In health this is about 1005ml/min • DO2 is reduced in cardiogenic and hypovolaemic shock (impaired contractility and reduced myocardial preload respectively)

  7. Oxygen transport Cardiac output 1.34 SaO2 CO DO2 [Hba] = x x x Arterial oxygen saturation Arterial haemoglobin concentration Oxygen content of 1g fully saturated haemoglobin Arterial Oxygen Content Oxygen Transport

  8. Oxygen uptake (VO2) • Amount of O2 taken up by the tissues • It is the difference between DO2 and O2 returned to lung in mixed venous blood • In health this is about 760 ml/min • An oxygen debt occurs when uptake exceeds delivery (as occurs in shock) and severity can be monitored by rising blood lactate (anaerobic metabolism)

  9. Septic Shock • Soluble cell bound receptors recognize microbial components or their toxins and stimulate release of pro-inflammatory and anti-inflammatory cytokines, complement, coagulation activation and platelet aggregation. • This results in vasodilatation and reduced intra-vascular volume (due increased vascular permeability) • Despite reduced contractility cardiac output is often increased in septic shock due to reduced afterload

  10. Septic Shock • Initially DO2 is elevated in septic shock primarily due to increased CO • However, VO2 is also raised due to increased metabolic activity of the tissues • When VO2 exceeds DO2 a lactic acidosis results • Untreated this leads to multi-organ failure

  11. Clinical presentation of septic shock • Hyperdynamic (unless significant hypovolaemia) • Proven source of infection • Hypotension • Signs of systemic inflammation (tachycardia, tachypnoea, hypo/perthermia, leuko-cytosis/paenia) • Confused, tachycardic, tachypnoeic, oliguric • Bounding pulses and warm peripheries

  12. Hypovolaemic and cardiogenic shock • Low cardiac output • BP can initially be normal due to compensatory sympathetic and neuro-hormonal mechanisms • Patients will be confused, pale, tachycardic, tachypnoeic, poor perfusion and oliguric • CVP low in HV shock • CVP high in CG shock with associated pulmonary oedema

  13. Investigations • Tailor to history and clinical findings. • FBC, Clotting, Electrolytes, Cr, Ur, Clotting, CRP, ABGs, lactate, troponin and blood cultures. • ECG, CXR. • ECHO (ventricular function, wall motion abN, valvular dysfunction, Tamponade, PE (spiral CT and pulmonary angiography)). • DPL, abdo USS, CT (concealed haemorrhage).

  14. Management • General measures for all patients with shock. • Specific appropraiate to aetiology.

  15. Target areas for treatment • Reduction of metabolic demands • Adequate O2 provision • Normalisation of filling • Manipulation of vasculature with Vasoactive agents • Normalization of SV • Manipulation of pump with Inotropes

  16. CAN WE REDUCE DEMAND? DO WE EVER DO IT?

  17. Yes! Yes!

  18. Management - Respiratory • High flow O2 (improve SaO2 and tissue DO2). • Ventilatory support or mechanical ventilation (reduces VO2 by resp muscles). • Early intubation facilitates invasive haemodynamic monitoring.

  19. VO2resp = Oxygen consumed by work of breathing • VO2tot = Total oxygen consumption

  20. VO2resp as percentage of VO2tot Intensive Care Med. 1995 Mar;21(3):211-7.

  21. So ventilatory support reduces oxygen demands In COPD, PS by mask can reduce this to almost zero

  22. Ventilatory support • CPAP: • Recruits alveoli • Improves V/Q • Improves oxygenation • Reduces work of breathing • BIPAP???

  23. Adequate sedation reduces oxygen demand Crit Care Med. 2003 Mar;31(3):830-3.

  24. 32 post- oesophagectomy/ head and neck malignancies • All buprenorphine -> Midazolam • light • mod • heavy sedation

  25. OXYGEN CONSUMPTION ml/min/m2

  26. Paralysis reduces muscle oxygen consumption Chest. 1996 Apr;109(4):1038-42.

  27. 8 patients • Mean age 63 years • Benzodiazipine + morphine • Then doxacurium paralysis • Mandatory ventilation • O2 consumption measured

  28. OXYGEN CONSUMPTION ml/min/m2 25% reduction

  29. Cooling reduces oxygen consumption Am J Resp Crit Care Med 1995 Jan;151(1):10-4

  30. 12 febrile, critically ill, mechanically ventilated patients • T down from 39.4 +/- 0.8 -> 37.0 +/- 0.50C OXYGEN CONSUMPTION ml/min

  31. HOW DO WE IMPROVE DELIVERY?

  32. 3 ways • Optimize O2 supplementation to patient • Optimization of Filling • Optimization of SV • Volume • Vasoactive drugs • Inotropes

  33. MANAGEMENT OF SHOCK • A: RECOGNISE WHAT TYPE OF SHOCK YOU • ARE DEALING WITH • B: CORRECT THE FILLING STATUS • Empty as a primary cause eg haemorrhage • Empty in sepsis due to increased capacitance • C: ONLY THEN USE VASO-ACTIVE AGENTS: • BETA-1 AGONISTS TO DRIVE THE HEART • ALPHA-1 AGONISTS OR COOLING TO VASOCONSTRICT • GTN OR WARMTH TO VASODILATE

  34. Targets? HISTORY • What BP is ‘normal’? CLINICAL • Cerebration • Peripheral perfusion MONITORING • Urine (0.5ml/kg/hr minimum) • ABG (degree of acidosis, trend) AIM FOR INDICES OF ADEQUATE ORGAN PERFUSION, NOT BP

  35. What is the type of shock? • Cardiogenic shock – pump failure • ischaemic / trauma / drugs • Hypovolaemic shock • haemorrhage • Low resistance circulatory / distributive shock • drugs / sepsis

  36. Bleed Diarrhoea Volume loss PE Fall in filling Tension PTx Tamponade Fall in cardiac contractility Burns FALL IN FLOW

  37. Basic Physiology PRESSURE = FLOW X RESISTANCE BLOOD PRESSURE = CARDIAC OUTPUT X RESISTANCE

  38. THE RESPONSE IS THE SAME… Efferent activity to Medulla falls Aortic arch and carotid sinus baroreceptors detect a drop in pressure Sympathetic efferents

  39. INCREASED SYMPATHETIC ACTIVITY CAUSES • VENOCONSTRICTION • INCREASES FILLING PRESSURE AND SUSTAINS • STROKE VOLUME • POSITIVE INOTROPIC EFFECT • SUSTAINS STROKE VOLUME • TACHYCARDIA • INCREASES CARDIAC OUTPUT • VASOCONSTRICTION • INCREASES RESISTANCE • PRESSURE = FLOW (UP) X RESISTANCE (UP)

  40. Management - Fluids • Optimize preload. • Restore circulating volume. • Large vols in HV/septic shock (latter - aim SvO2 >70% / Hb >10g/dl reduce hosp mort by 16%). • Judicious vols in CG shock (PAoP/CI).

  41. Under filled Well filled Over filled >3mmHg 20mmHg 3mmHg <3mmHg Filling 200ml COLLOID CHALLENGE Stroke volume PAWP Blood volume Blood volume

  42. LVF: Physiology Pulmonary Veins Pulmonary Capillaries LA MV At end-diastole, MV is open, flow has ‘ceased’ SO LVEDP = LAP = PVP = PCP = HYDROSTATIC PCP LV

  43. Management - Fluids • CVP surrogate for preload • Oesophageal doppler better measure of filling • Fluid should be used to replace that lost • Aim Hb 7-9 g/dl • Higher mortality if aim Hb 10-12 g/dl.

  44. Management - Fluids • Crystalloid vs Colloid….. • Colloids restore circ vol more efficiently, but no worse outcome with crystalloid only • Systematic review colloid use – 4% increase in mortality (esp HAS) • SAFE study • Hypertonic solutions may be useful in pts with cerebral oedema requiring fluid resuscitation and may reduce fluid and Blood Tx requirements.

  45. Management - Inotropes • HV shock – rarely needed – fluids alone restore CO and BP • CG shock – fluids not helpful, inotropes needed • Septic shock – fluids needed as well as inotropes • Both require vasoactive drugs to improve tissue perfusion and reverse tissue hypoxia.

  46. Inotropic support RV SV (ml) LV 60 5 10 Filling pressure (mmHg)

  47. Management - Inotropes • CG shock – (low CO/BP and elevated SVR). • Inodilator (Dobutamine/Milrinone) if BP not too low. • Inodilator plus inoconstrictor (Adrenaline/Dopamine) or vasopressor (NorAdr) if BP compromised. • Adr S/E – hyperglycaemia/hypokalaemia/hyperlactataemia (interpret Lactate levels with caution).

  48. Management - Inotropes • Septic shock – (high CO low BP from peripheral vasodilatation). • Firstly optimize preload. • Then use vasopressor (NorAdr) • If CO is reduced consider adding Dobutamine. • Dopamine (inoconstrictor) could be used but associated with adverse effects on pituitary (reduced prolactin/GH/TRH), T-cell function, gut mucosa perfusion and renal medullary VO2.

  49. Doses • Dobutamine (5-20µg/kg/min) • adjust by 2.5µg/kg/min increments • Adrenaline (start at 0.05µg/kg/min) • adjust by 0.02µg/kg/min increment • GTN to lower resistance

  50. Hypovolaemic shock • In case of haemorrhagic shock – stop the bleeding (surgery/radiology/endoscopy) • Fluid resuscitation • Correct hypovolaemia/hypoxia/anaemia and increase DO2 prior to surgery to reduce peri-operative mortality

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