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Vasoactive agents (4).pptx
- 1. Vasoactive agents Dr KIRUBELTINSAE MD Assistant professor in Anesthesiology and critical care
- 2.
- 3. • A 65yrs. old male patient with esophageal ca procedure-m esophagectomy Vital signs- BP-7040 HR-90 SaO2-99 What is your next step?
- 4. • A 32years old female, known cardiac patient for the last 11 years. came with cardiogenic shock • Preferred choice of vasoactive agent is……?
- 5. Definitions • Pressor: Increasesblood pressure by stimulating constriction of blood vessels • Increases vascular tone • Inotrope: Alters force or energy of muscular contractions • Positive: Increases myocardial contractility • Chronotropic-increase heart rate
- 6. The autonomic nervoussystem • Responsible for maintaining normal functions such as • blood pressure and blood flow. • It has two divisions; • the parasympathetic and the sympathetic systems. • The parasympathetic • conservation of energy and maintenance of organ function during periods of minimal activity, • The sympathetic acts when the ‘fight or flight’ response is required.
- 7. • The parasympatheticnervous system • to regulation of heart function through the vagus nerve where it slows the rate • has little or no control over the blood vessels. • The sympathetic nervous system • An excitatory influence on heart rate and contractility and • controls the smooth muscle tone of the blood vessels. • The increases in sympathetic activity will increase the constriction or visa versa.
- 8. • The maintypes of adrenergic receptors are • alpha (α), beta (β) and dopamine (DA), • Generally, α receptors cause constriction, while β cause dilation and increased contractility. • Some blood vessels are supplied with both these constrictor and dilator receptors.
- 9. • An adrenergicagonist is a drug that stimulates a response from the adrenergic receptors. • Inotropes are agents that increase myocardial contractility (inotropy) • e.g. adrenaline, dobutamine, dopamine. • Vasopressors are agents that cause vasoconstriction leading to increased systemic and/or pulmonary vascular resistance (SVR, PVR) • e.g. noradrenaline, metaraminol. • Inodilators are agents with inotropic effects that also cause vasodilation leading to decreased SVR and/or PVR e.g. dobutamine.
- 10. • 1 heartand 2 lungs’ refers to • α1 and β1 being found in the heart, • α2 and β2 will be found in the lungs • α1 and β2 will be found in blood vessels
- 11. Type Tissue Actions Alpha1 (α1) Most vascular smooth muscle Constriction Heart Increased force of constriction (inotropy) Alpha 2(α2) Vascular adreneric nerve terminals Inhibition of sympathetic activity. Has central and peripheral effects – BP ↑ or ↓ Beta 1(β1) Heart Increased rate (chronotropy) and force of contraction Beta 2(β2) Bronchi, uterine and vascular smooth muscle Relaxation – causes dilation Beta 3(β3) Heart Increased force of contraction in healthy heart Cardioprotective in heart failure – has negative inotropic effect Dopamine (DA1) Vascular bed of brain, splanchnic organs<, kidneys and coronary arteries Increases peripheral resistance (vasoconstriction) but can vasodilate renal and gut circulation. Can also increase vascular resistance systemically
- 12. Receptor Alpha 1Beta 1 Beta 2 DA1 Metaraminol +++ + 0 0 Adrenaline (epinephrine) +/++ ++ + 0 Noradrenaline (norepinephrine) +++ +++ + 0 Phenylephrine ++ 0 0 0 Dobutamine + ++ +/++ 0 Dopamine ++ + 0 +++ Dopexamine 0 + +++ ++ Ephedrine ++ ++ 0 0
- 14. Shock • Inability ofoxygen delivery to meet tissue oxygen requirements • Hypovolemia (decreased circulating volume) • Cardiac function impairment (decreased myocardial contractility) • Inappropriate distribution of cardiac output secondary to abnormal vasodilatation
- 15. • Cardiac output •Heart Rate • Sympathetic and Parasympathetic tone • Circulating chatecolamines • Preload • Changes in venous return • Changes in plasma volume • Contractility • Sympathetic tone • Circulating catecholamines
- 16. Septic shock • Hypotensiondespite adequate fluid resuscitation • Presence of hypoperfusion or organ dysfunction • Acidosis / alteration in mental status • Sepsis: temp >38°C or <36°C; HR> 90 bpm* respiratory rate>20 breaths/min, need for mechanical ventilation; WBC 12,000*
- 17. Cardiogenic shock • Pumpfailure • Results when more than 40% of myocardium damaged • Similar circulatory and metabolic changes to hemorrhagic shock
- 18. Treatment 1. Fluids /Procedures 2. DRUGS! • Vasopressors • Inotropes
- 19. Vasopressor • Norepinephrine • 0.01mcg/kg/min-3mcg/kg/min •Dopamine • 5-10 mcg/kg/min-Renal Dose • 10-20mcg/kg/min-cardiac dose • 20-40 mcg /kg/min :vascular dose • Epinephrine • 0.01mcg/kg/min -1mcg/kg/min • Vasopressin • 10IU-40 IU • Phenylephrine • 0.15-1mcg/kg/min
- 20. Phenylephrine • Selective α1-adrenergicagonist • Rapid onset • Short duration • Primary vascular effects • Second line in septic shock Indicated in other distributive shock • Spinal shock • Medication induced hypotension
- 21. Summary • Perfusion adequacyis important!!! • Restore effective tissue perfusion (In all organs) and normalize cellular metabolism