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‘Cures For A Broken Heart’

‘Cures For A Broken Heart’. Cardiogenic Shock, IABP, Vasopressors, Inotropes & Cardiologists Daniel Orr. The Problem. Definition ‘Decreased cardiac output and evidence of tissue hypoxia in the presence of adequate intravascular volume.’ Clinically

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‘Cures For A Broken Heart’

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  1. ‘Cures For A Broken Heart’ • Cardiogenic Shock, IABP, Vasopressors, Inotropes & Cardiologists Daniel Orr

  2. The Problem • Definition • ‘Decreased cardiac output and evidence of tissue hypoxia in the presence of adequate intravascular volume.’ • Clinically • Cool, mottled extremities, poor capillary return • Clouded sensorium • Hypotension • Oliguria • Pulmonary ‘Congestion’ • Exclusion of other causes

  3. The Problem • Definition • Haemodynamic criteria • SBP <90mmHg >30min • CI <2.2L/min m2 • PCWP >15mmHg Hollenberg, SM. Kavinsky, CJ. Ann Intern Med. 1999;131:47-59

  4. The Problem • Incidence • Range 5 – 10% patients presenting with AMI • Does not account for out of hospital arrests/death

  5. The Trigger • Cause & Epidemiology • Myocardial Infarct • Majority of cases – Pump failure • Include right ventricular infarct • Mechanical Events • Acute MR • Rupture IVS or free wall • Myocardial Dysfunction • Myocarditis, Cardiomyopathy, Septic Shock, Prolonged CPB

  6. Risk Factors & Evolution • Shock • More likely in those with anterior and previous infarct, old, the diabetic, PVD, CVA • Time Course • Of those reaching hospital minority of patients in shock ~ 10% • 7 hours typical delay between infarct and symptomatic shock

  7. The Breakdown • Pathophysiology • Described as a downward spiral of events of compounding events • Key Elements • Primary Pump Failure • Sympathetic Nervous System Activation

  8. The Breakdown • Pathophysiology • Pump Failure • Both systolic & diastolic components • Systolic • Reduction in stroke volume, therefore cardiac output • Remainder of myocardium hypercontractile, increasing O2 consumption • Significant dependence on coronary flow, potentially already compromised by disease • All worsen ischaemia

  9. The Breakdown • Pathophysiology • Pump Failure • Diastolic • Perfusion reduced by hypotension and SNS induced tachycardia • Increased EDP additionally reduces perfusion • Increased wall stress increases O2 consumption • All worsen ischaemia

  10. The Fallout • Pathophysiology • Sympathetic Activation • Attempt to maintain organ perfusion • Results • Tachycardia • Increased circulating catecholamines • Activation of RAA system • Consequences • Increased myocardial O2 demand via HR, contractility, afterload • Increased preload via RAA • Worsening ischaemia & Pulmonary consequences

  11. The Fallout • Pathophysiology • Tissue Hypoxia • Results in increased products of anaerobic metabolism including lactate, and a decrease in pH • Worsens myocardial performance • The Latest • Systemic inflammatory response • Cytokines, interleukins, inducible NO synthase • Consequences for genesis, treatment & outcome

  12. Assessing The Damage • Symptoms & Signs • Emergency - ‘Time is muscle’ (or Tissue) • Signs of inadequate tissue perfusion • CVS including elevated JVP, pulmonary oedema, extra heart sounds, murmur, arrhythmia • Echo - wall motion, papillary muscle, valvular function • Invasive monitoring

  13. Damage Control • Initial Management • General Supportive • Infarct • Shock

  14. Damage Control • Initial Management • General Supportive • Correct hypoxia / acidosis • Relieve pain • Correct electrolytes

  15. Damage Control • Initial Management • Infarct • Aspirin • Clopidogrel • Heparin • GPIIb/IIIa inhibitors • NSTEMI

  16. Damage Control • Initial Management • Infarct • Thrombolysis / PTCA / CABG / VR • Avoidance of agents with negative inotropic effects - beta blockers, calcium channel blockers

  17. Damage Control • Initial Management • Shock • Volume resuscitation, especially if cause is due to RV infarction • Guided by Sats, MAP, CO, PCWP - aim for lowest value to give highest CO. Often 18-25mmHg • Pulmonary oedema • Diuretics • Vasodilators

  18. Invasive monitoring • All modalities should be considered • Arterial line - almost universal • Central line - required for administration of inotropes • PA catheter / PiCCO • Refractory hypotension • Mechanical complications & cause • Vasopressor / Inotropic agents

  19. Putting The Squeeze On • Vasopressors & Inotropes • Vasopressors • Agents that produce vasoconstriction • Mostly sympathomimetics, catechol and non-catecholamines • Directly acting agents • Inotropes • Agents that increase myocardial contractility • Sympathomimetics • Phosphodiesterase inhibitors • Others

  20. Putting The Squeeze On • First Line • Dopamine • Noradrenaline • Second Line • Dobutamine • Milrinone

  21. Putting The Squeeze On • First Line • Dopamine • Naturally occuring sympathomimetic amine, with effects at α, β, and DA receptors • Low dose β effects predominate, high does α • Both vasoconstrictor and inotropic effects • Increases PCWP • Risk of arrhythmia (>NA latest NEJM) • Tachycardia, increased O2 demand

  22. Putting The Squeeze On • First Line • Noradrenaline • Potent naturally occurring sympathomimetic amine and neurotransmitter, with effects at α & β receptors • Predominant α effects • Tissue necrosis • Risk of arrhythmia • Adrenaline - substitute for Dopamine

  23. Putting The Squeeze On • First Line • Considerations • Vasopressors typically increase SVR, with limited direct effect on CO • Increased SVR may worsen CO - consider invasive monitoring

  24. Putting The Squeeze On • Second Line • Dobutamine • Synthetic catecholamine, predominantly β effects • Increases inotropy and chronotropy, often of benefit in cardiac failure • May worsen hypotension • Risk of arrhythmia • Can be combined with Dopamine

  25. Putting The Squeeze On • Second Line • Milrinone • Selective PDE III inhibitor inotropic agent • Increases CO via increased cAMP • Additionally has vascular vasodilating effects • Risk of hypotension and arrhythmia • No studies to demonstrate benefit

  26. Party Time • IABP & other VADs • Benefit of improving coronary perfusion and cardiac performance • Reduce myocardial ischaemia & cardiac work • Do not alter SVR

  27. Party Time • IABP • Description • Intravascular counterpulsation device used to augment cardiac function • Haemodynamic Effects • Displacement of blood into proximal aortic territory during diastole • Increases coronary & cerebral blood flow • Reduction in afterload 2o to ‘vacuum’ effect • Reduces cardiac work

  28. Party Time • IABP • Consequences • Improved myocardial O2 supply and reduced O2 demand • Improvement in end organ function, reduction in acidosis • In cardiogenic shock used as adjunct to definitive treatment. In isolation does not improve mortality

  29. Party Time • IABP • Uses/Indications • Cardiogenic shock • Including AMI & mechanical lesions eg MR • Support post PTCA • Weaning from CPB • Refractory unstable angina / High risk restenosis PTCA or thrombolysis

  30. Party Time • IABP • Contraindications • Absolute • Moderate & Severe Aortic Regurgitation • Dissecting Aortic Aneurysm • Relative • PVD • AAA

  31. Party Time • IABP • Complications • Vascular • Limb ischaemia • Vascular laceration • Major Haemorrhage • Non-Vascular • Embolization • Balloon migration & ischaemia cerebral, renal • Sepsis • Balloon rupture

  32. Party Time • IABP • Complications • Other • Haemolysis • Thrombocytopaenia • Peripheral neuropathy • Practical • Anticoagulation • Post CABG • AMI

  33. Party Time • IABP • Practical • Triggering • ECG • Pacing • Arterial pressure • Monitoring • Peak diastolic will be higher than systolic (augmented) • Continue to use MAP on IBP to guide ‘tropes’

  34. Party Time • IABP • Practical • Modes - 1:1, 1:2, 1:4 • Size does matter • Differing volume of balloon for height • Weaning • Stable haemodynamics typically after 24-48/24 • Reduce inflation ratio, off after ~ 2/24 at 1:4

  35. Finding Solutions • Definitive Treatment • Thrombolysis • Revascularization • CABG / VR

  36. Finding Solutions • Definitive Treatment • Thrombolysis • Evidence suggests benefit over placebo in cardiogenic shock, improved survival • Use in combination with IABP • PTCA and CABG superior • Consider in patients who are high risk, in areas without angiographic services

  37. Finding Solutions • Definitive Treatment • Revascularization • Mainstay of AMI induced cardiogenic shock • Early intervention preferable • Improvement in both infarct and remote myocardium • Response may be variable, and not immediately apparent

  38. Finding Solutions • Definitive Treatment • CABG / VR • Benefit demonstrated inlimited capacity in trials • Relatively low mortalityrate • Significant logisticalchallenges • Typically limited to thosewith mechanical causesof cardiogenic shock

  39. Going Back For Seconds • Why Treatment Works • Stunning • Hibernation

  40. Moving On • Outcomes • High mortality • Limited scope forrecovery

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