1 / 40

Pharmacologic Management of Acute Circulatory Failure: Vasoactive Medications

Pharmacologic Management of Acute Circulatory Failure: Vasoactive Medications. Thank you Suanne Daves, MD. What you will hear today. A short review of Shock

mio
Download Presentation

Pharmacologic Management of Acute Circulatory Failure: Vasoactive Medications

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Pharmacologic Management of Acute Circulatory Failure: Vasoactive Medications Thank you Suanne Daves, MD

  2. What you will hear today A short review of Shock A look at how the intrinsic sympathetic nervous system & various drugs that can accelerate/enhance the excitation-contraction coupling phenomenon in myocytes (improve cardiac output).

  3. Circulatory Failure / Shock What is it? Metabolic demand outstrips supply or the ability to extract The anaerobic state leads to accumulation of lactic acid. Energy dependent cellular processes cease Cellular edema, cellular disruption, cell death….. Organ failure

  4. Chronotropy HR x SV Volume Inotropy EDV - ESV Lusiotropy Afterload BP = CO x SVR

  5. BP = CO x SVR SVR = vascular tone

  6. A digression to cell biology Cardiac Output and SVR are all about Calcium

  7. all about Calcium PDE

  8. Back to something more familiar: Starling

  9. The Body’s Neuronal Defense System

  10. β1 β2 ά1 β2 ά1 β2 Vasopressin DA1-2 Vasopressin

  11. Bohn (2006). Inotropic Agents in Heart Failure. Heart Failure in Children and Young Adults. Chang & Towbin.

  12. PDE

  13. When you need to intervene: Vasoactive Medications: Goals of treatment Provide adequate tissue oxygenation. Maintain vital organ function. Restore systemic blood pressure. Tailor drugs to minimize adverse side effects.

  14. Vasoactive Medications • Catacholamines • Vasopressin • Phosphodiesterase inhibitors • Calcium sensitizers

  15. Catacholamines with inotropic properties • Epinephrine • Norepinephrine • Isoproterenol • Dopamine • Dobutamine

  16. Bohn (2006). Inotropic Agents in Heart Failure. Heart Failure in Children and Young Adults. Chang & Towbin.

  17. Bohn (2006). Inotropic Agents in Heart Failure. Heart Failure in Children and Young Adults. Chang & Towbin.

  18. Bohn (2006). Inotropic Agents in Heart Failure. Heart Failure in Children and Young Adults. Chang & Towbin.

  19. Bohn (2006). Inotropic Agents in Heart Failure. Heart Failure in Children and Young Adults. Chang & Towbin.

  20. Bohn (2006). Inotropic Agents in Heart Failure. Heart Failure in Children and Young Adults. Chang & Towbin.

  21. Starling again Improved inotropy CO

  22. Catacholamines with pressor properties • Phenylephrine • Epinephrine • Norepinephrine • Dopamine

  23. More Starling…more preload = more CO Remember: too much afterload = CO

  24. Other Vasoactive Options • Milrinone • PDE inhibitor • Vasopressin • Vasoconstriction • Improves sensitivity to catachols • Levosimendan • Calcium sensitizing agent

  25. Starling again Reduced afterload improved CO

  26. The Downside of Vasoactive Agents(mostly true for catachols) • Increased myocardial O2 demand • Myocardial injury/cell death • Tolerance/tachyphylaxis • Arrhythmogenesis • Peripheral vasoconstriction • Elevates SVR • Compromises splanchnic blood flow

  27. A 4-mos-old infant presents to the ER with irritability, poor po intake, and tachypnea. The ER doc says the baby looks “shocky”. They have started an IV & given 20mL/kg NS. Bedside Reality…

  28. The infant is awake & quiet. HR: 170s-180s (sinus) RR: 70s BP: 90/68 He is cool peripherally. His pulses are ‘thready’ pH 7.29/pCO2 38/pO2 82/HCO3 18 Lactate 4.0 Would you begin an inotrope/pressor? Which one?

  29. Same infant………. HR: 180s (sinus) RR: 70s BP: 52/44

  30. Key Concepts The predominant β-AR in the heart is the β1-AR (<75%). β2-ARs are largely found in vascular smooth muscle. Ά1-ARs predominate in vascular smooth muscle although they are present in the neonatal myocardium.

  31. Key Concepts Catacholamines are good in the short term for hemodynamic support but most increase myocardial oxygen demand, increase diastolic pressures, and can lead to apoptosis PDE inhibitors, while increasing intracellular Ca+, are lusiotropic and inotropic agents that do not increase myocardial O2 demand and are not associated with tachyphylaxis.

  32. Key Concepts A strategy of combining a PDE inhibitor with a catecholamine may be the best approach to support of the myocardium and circulation. Most inotropic agents to date have a common final intracellular pathway of increased intracellular Ca+, which may ultimately lead to cell (myocyte) death.

  33. And we continue to look for something better A new generation of inotropic agents known as calcium-sensitizing agents achieve their positive inotropic effects without an increase in intracelluar Ca+ or myocardial O2 consumption. Unfortunately they early studies of the first of these drugs demonstrated less benefit than was anticipated Levosimendan

  34. β1 β2 1

More Related