Uppers downers and squeezers

1,323 views

Published on

Presentation on inotropic and vasoactive drugs

Published in: Health & Medicine
0 Comments
3 Likes
Statistics
Notes
  • Be the first to comment

No Downloads
Views
Total views
1,323
On SlideShare
0
From Embeds
0
Number of Embeds
59
Actions
Shares
0
Downloads
30
Comments
0
Likes
3
Embeds 0
No embeds

No notes for slide

Uppers downers and squeezers

  1. 1. Uppers, Downers and SqueezersINOTROPES AND VASOACTIVE DRUGS
  2. 2. Aim and Objective Functional overview of how inotropes and vasoactive drugs work. Explore nursing considerations. Discuss case examples. Hopefully end up feeling more confident.
  3. 3. It’s all about the Oxygen For tissues to be oxygenated, 3 factors need to be considered:  1) Oxygen transfer across the alveolar-capillary membrane  2) Oxygen attachment to haemaglobin  3) Adequate cardiac output (CO) to move the oxyhaemaglobin compound to the tissues – this is what we are talking about!
  4. 4. Two Limbs to Oxygenation
  5. 5. To increase CO we can…1) Enhance circulating volume through fluidresuscitation (increasing preload)2) Enhancing myocardial contractility with inotropes(their inotropic effect)3) Manipulating heart rate with inotropes (theirchronotropic effect)
  6. 6. Remember Cardiac output (CO) =Heart Rate (HR) x Stroke Volume (SV)
  7. 7. Measuring Cardiac Output How do we commonly evaluate? How complex is this?
  8. 8. Blood PressureBP = CO x Total Peripheral ResistanceSimple enough right???
  9. 9. Remember this?
  10. 10. Stroke Volume Complex beast affected by preload, afterload and contractility. Confused???
  11. 11. How does this stay balanced?Parasympathetic down regulates and Sympathetic up regulates.
  12. 12. A&P
  13. 13. It’s all about the ReceptorsTable 1. Adrenergic receptor sites (SNS)Receptor Actions Locationsα ↑SVR Coronary arterioles ↑Blood pressure Vascular smooth muscle ↓Insulin releaseβ1 ↑Heart rate Sinoatrial node ↑Contractility Myocardiumβ2 ↑Contractility Coronary arterioles ↓SVR Bronchial smooth muscle Atrioventricular node Vascular smooth muscleDA Vasodilation Kidney Mesentery HeartSVR =systemic vascular resistance. DA = Dopaminegic
  14. 14. Important terms – Agonist
  15. 15. Important terms - Antagonist
  16. 16. Important terms – Partial Agonist
  17. 17. Ok take a breather!
  18. 18. How do we treat this stuff?http://www.youtube.com/watch?v=HMGIbOGu8q0
  19. 19. Let’s talk drugs!In the context of the SNS, drugs:Mimic or impair (stimulate or block) Directly (agonist or antagonist) Indirectly - releasing endogenous Norad (metaraminol, ephedrine at a1)
  20. 20. Let’s talk drugs!In the context of the PNS,drugs work on: Nicotinic and muscarinic receptors with Ach as neurotransmitter M2 heart
  21. 21. Atropine - PNS Anticholinergic drug – works as a competitive antagonist in muscarinic receptors (M2 = Heart) Blocks slow – down signals to the heart.
  22. 22. Adrenaline - SNS Non-selective b and a agonist +inotrope and chronotrope Vasodilates at low dose, constricts at high dose Bronchial smooth muscle relaxant Use in asthma?
  23. 23. Noradrenaline - SNS Acts predominantly on alpha-receptors and beta- receptors in the heart. Causes peripheral vasoconstriction (alpha- adrenergic action) and a positive inotropic effect on the heart and dilatation of coronary arteries (beta- adrenergic action). Why is it important to assess adequate fluid loading?
  24. 24. Dobutamine - SNS Direct acting inotropic whose primary activity results from stimulation of the beta-receptors of the heart while producing comparatively mild chronotropic, hypertensive, arrhythmogenic and vasodilative effects. It does not cause the release of endogenous noradrenaline as does dopamine Used for heart failure for the above reasons 250mg vials
  25. 25. Vasopressin (ADH) increase resorption of water by the renal tubules Cause contraction of smooth muscle of the gastrointestinal tract and of all parts of the vascular bed, especially the capillaries, small arterioles and venules, with less effect on the smooth musculature of the large veins. 20IU/ml
  26. 26. Metaraminol - SNS Increases both systolic and diastolic blood pressure. The pressor effect begins one to two minutes after intravenous injection, and lasts about 20 minutes to one hour. Positive inotropic effect on the heart and has a peripheral vasoconstrictor action. Potent sympathomimetic – alpha agonist effects, mild beta 1 effects.
  27. 27. Ephedrine – SNSStimulates both alpha and beta-adrenergicreceptors indirectly and also releases endogenousnoradrenaline from its storage site (particularlyobserved in the substantia nigra).Often used in OT due to strong direct evidencebase lying in anaesthetic hypotension.
  28. 28. Phenylephrine - SNSUsed mostly in OTProduces vasoconstriction that lasts longer than that ofadrenaline and ephedrine.Responses are more sustained than those to adrenaline,lasting 20 minutes after intravenous and as long as 50minutes after subcutaneous injection.Its action on the heart opposite to adrenaline andephedrine, in that it slows the heart rate and increasesthe stroke output, producing no disturbance in therhythmPowerful postsynaptic alpha-receptor stimulant withlittle effect on the beta-receptors of the heart.A singular advantage of this drug is the fact that repeatedinjections produce comparable effects.
  29. 29. GTN – Direct Vasoactive Glyceryl trinitrate produces a dose related dilation of both arterial and venous beds. Decreases venous return to the heart, reducing left ventricular end diastolic pressure and pulmonary capillary wedge pressure (preload). Arteriolar relaxation reduces systemic vascular resistance and arterial pressure (afterload). Also dilates the coronary arteries, although this effect is short-lived.
  30. 30. These are also out there Some less frequently used drugs
  31. 31. Dopamine - SNS Stimulates alpha, beta and dopamine receptors. Precursor to noradrenaline chemically At infusion rates of 0.5 to 2 microgram/kg/minute, dopamine receptors are selectively activated and blood pressure either does not change or decreases slightly. Causes renal and mesenteric vasodilatation - Renal plasma flow, glomerular filtration rate and sodium excretion usually increase. At infusion rates of 2 to 10 microgram/kg/minute, beta1- receptors are activated and cardiac output and systolic blood pressure increase. The total peripheral resistance is relatively unchanged because of peripheral vasoconstriction (alpha effect) and muscle vasodilatation (beta effect). At infusion rates above 10 microgram/kg/minute, alpha- receptors are activated, causing vasoconstriction, and both systolic and diastolic pressures increase 200mg Ampoules
  32. 32. IsoprenalineActs on the heart, smooth muscle of bronchi,skeletal muscle vasculature and gastrointestinaltract.Increases cardiac output due to its positiveinotropic and chronotropic actions and byincreasing venous return.Also lowers peripheral vascular resistance.The rate of discharge of cardiac pacemakers isincreased.Great option in complete heart block.
  33. 33. MilrinoneSelective phosphodiesterase inhibitor which haspositive inotropic and vasodilatory activity.Milrinone improves hemodynamics andbiventricular function in patients withventricular dysfunction by increasing strokevolume index, increasing left ventricularcontractility, producing pulmonary vasodilation.Used in heart failure due to minimalchronotropic effect
  34. 34. Sodium Nitroprusside (SNP) – Direct Vasoactive Potent relaxation of vascular smooth muscle and consequent dilatation of peripheral arteries and veins. Non-selective compared to GTN .
  35. 35. LevosimendanDeveloped for the treatment of decompensated heartfailure and is used intravenously when patients withheart failure require immediate initiation of drugtherapy.It increases the sensitivity of the heart to calcium, thusincreasing cardiac contractility without a rise inintracellular calcium.Exerts its effect by increasing calcium sensitivity ofmyocytes by binding to cardiac troponin C in a calcium-dependent manner.It also has a vasodilatory effect, by opening adenosinetriphosphate (ATP)-sensitive potassium channels invascular smooth muscle to cause smooth musclerelaxation.
  36. 36. Ok……. Inotropic drugs are potentially dangerous so be very thorough checking. Vascular access needs to be spot on. On central line always endeavour to use distal, brown lumen (in furthest) Wear gloves when preparing. Know what the drug does and why we use it. Don’t EVER make a mistake with inotropes!!!

×