inotropes and vasopressors.ppt
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Inotropes and Vasopressors.pptTRANSCRIPT
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Inotropes&
Vasopressorsmanagement of various types of
shock.
DR.MUHAMMAD ALI YOUSUF
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Definitions
• Inotropes:• Agents administered to increase
myocardial contractility and therefore cardiac index
• Vasopressor• Agents are administered to increase
vascular tone and thereby elevate mean arterial pressure (MAP).
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Inotropes Vs. Vasopressors
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Inotropes• Drugs that affect the
force of contraction of myocardial muscle
• Positive or negative
• Term “inotrope” generally used to describe positive effect
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Vasopressor
• Drugs that stimulates smooth muscle contraction of the capillaries & arteries
• Cause vasoconstriction & a consequent rise in blood pressure
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Main Goal
Tissue perfusion & oxygenation
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Physiological Principles
MAP = CO x SVR
CO = HR x SV
Preload Contractility Afterload
~ 1
r4
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Basic principles - Vasopressors
MAP = CO x SVR
CO = HR x SV
Preload Contractility Afterload
~ 1
r4
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Basic principles - Inotropes
MAP = CO x SVR
CO = HR x SV
Preload Contractility Afterload
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Mixed action drugs
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Use of inotropes & vasopressors
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Drug Classification• Sympathomimetics
• Naturally occurring• Synthetic
• Other inotropes• cAMP dependent• cAMP independent
• Other vasopressors
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Sympathomimetics• Drugs that stimulate adrenergic receptors
• G-protein coupled receptors
G - ProteinActivation of intermediate messenger
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Main classes of Adrenoceptor receptors
1
• Located in vascular smooth muscle• Mediate vasoconstriction
2
• Located throughout the CNS, platelets• Mediate sedation, analgesia & platelet
aggregation
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Main classes of Adrenoceptor receptors
1
• Located in vascular smooth muscle• Mediate vasoconstriction
2
• Located throughout the CNS, platelets• Mediate sedation, analgesia & platelet aggregation
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Main classes of Adrenoceptor
receptors1
• Located in the heart• Mediate increased contractility & HR
2
• Located mainly in the smooth muscle of bronchi
• Mediate bronchodilatation
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Main classes of Adrenoceptor
receptors1
• Located in the heart• Mediate increased contractility & HR
2
• Located mainly in the smooth muscle of bronchi• Mediate bronchodilatation• Located in blood vessels
• Dilatation of coronary vessels• Dilatation of arteries supplying skeletal muscle
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β1 Adrenoceptor
G - Protein Adenyl cyclase
ATP cAMPIncreased
heart muscle contractility
Adrenaline
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Sympathomimetics
• Naturally occuring• Epinephrine• Norepinephrine• Dopamine
• Synthetic• Dobutamine• Dopexamine• Phenylephrine• Metaraminol• Ephedrine
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Uses• Are used in critically ill patients with
profound hemodynamic impairment to such extent that tissue perfusion is not sufficient to meet metabolic requirements.
• They are administered via a large central vein .
• To explore the evidence for their use in clinical practice.
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Common Inotropes and Vasopressors
• Catecholamines:• Dopamine• Adrenaline• Noradrenaline• Dobutamine• Isoprenaline• Phenylephrine
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Common Inotropes and Vasopressors
• Vasopressin
• Phosphodiesterase inhibitors
• Calcium sensitizing agents
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Catecholamines:
• Endogenous:(adrenaline, noradrenaline, dopamine)
• Synthetic:(dobutamine, Isoprenaline, phenylephrine)
• mediate their cardiovascular actions predominantlythrough α1, β1, β2 and dopaminergic receptors.
• The density and proportion of these receptors modulates the physiological responses of inotropes and vasopressors in individual tissues.
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Catecholamines:• β1 receptor is found predominantly on myocardium and
stimulation of which results inenhanced myocardial contractility through Ca2+ mediated facilitation of the actin-myosin complex binding with troponin C and enhanced chronicity through Ca2+ channel activation
• β2 receptor stimulation on vascular smooth muscle cells through a different intracellular mechanism results in increased Ca2+ uptake by the sarcoplasmic reticulum and vasodilation
• Activation of α1 receptors on arterial vascular smooth muscle cells results in smooth muscle contraction and increase in systemic vascular resistance.
• Stimulation of dopaminergic receptors (D1 and D2) in the kidney and splanchnic vasculature results in renal and mesenteric vasodilatation
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Dopamine
• Effect dose dependent• Direct
• Low dose - 1
• High dose - 1
• Indirect• Stimulates norepinephrine release
• D1 receptors• Vasodilatation of mesenteric & renal circulation
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Dopamine
• Acts on both dopaminergic and adrenergic receptors
• At low doses (0.5-3.0 μg/kg/min), dopamine acts predominantly on D1 receptors in the renal, mesenteric, cerebral and coronary beds resulting in selective vasodilation.
• Some reports suggest that dopamine increases urine output by augmenting renal blood flow and glomerular filtration rate and natriuresis by inhibiting aldosterone and renal tubular transport
• But the clinical significance of “renal-dose” dopamine is somewhat controversial because a renal protective effect has not been demonstrated
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Dopamine• At intermediate doses (3-10 μg/kg/min), also
stimulates β1 receptor and increases cardiac output (CO), predominantly by increasing stroke volume with variable effect on heart rate.
• At higher dose (10-20 μg/kg/min), the predominant effect is to stimulate α1-adrenergic receptors and produce vasoconstriction with an increased systemic vascular resistance (SVR),and the sum of these effects is an increase in mean arterial pressure (MAP).
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Adrenaline
• Stimulates & receptors• Predominantly effects at low doses
and effects at high doses
• Clinical uses• Cardiac arrest• Anaphylaxis• Low cardiac output states• Upper airway obstruction• Combination with local anaesthetics
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Low Dose Adrenaline
• Adrenaline is a potent agonist for β1, β2 and α receptors present in cardiac and vascular smooth muscle.
• Low dose of adrenaline increases cardiac output because of β1 receptor mediated inotropic and chronotropic effects.
• The α-receptor mediated vasoconstriction is often offset by the β-2 receptor mediated vasodilation.
• The result is an increased cardiac output with decreased SVR and variable effect on the MAP.
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Higher dose • α-receptor mediated vasoconstriction predominates
which results increased SVR in addition to increased CO.
• Arterial and venous pulmonary pressure are increased through direct pulmonary vasoconstriction and increased pulmonary blood flow and hence right ventricular after load.
• Adrenaline has been shown to increase lactate concentration especially in severe infection and increases oxygen consumption.
• The rise in lactate is of clinical importance as lactate is utilized as a marker of tissue hypo-perfusion.
• The increase in serum lactate induced by adrenaline does not associated with harm.
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Norepinephrine
• Predominantly stimulates 1 receptors
• Most commonly used vasopressor in critical care
• Very potent• Administered by infusion into a central vein
• Uses• Hypotension due to
vasodilatation• Septic shock
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Noradrenaline
• Noradrenaline is a potent α1-adrenergic receptor agonist with modest β-agonist activity.
• However, it has shown effects on contractility in critical illness.
• It primarily increases systolic, diastolic and pulse pressure and has a minimal net impact on CO.
• It has minimal chronotropic effects because of which it is a drug of choice in settings where heart rate stimulation is undesirable.
• Coronary flow is maintained to certain extent because of its vasoconstrictor effects.
• High doses of noradrenaline can be safely used to maintain cerebral perfusion pressure without significantly compromising the circulatory flow.
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Dobutamine
• Synthetic
• Predominantly 1
• Small effect at 2
• Uses• Low cardiac output
states• Cardiogenic shock
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Dobutamine
• Dobutamine is a synthetic analogue of dopamine, binding in a 3:1 ratio to β1 and β2 receptor respectively.
• It is a potent inotrope with weaker chronotropic activity.
• Combined α1 receptor agonsim and antagonism as well as β2 stimulation such that the net vascular effect is often mild vasodilation, particularly at lower dose (≤5 μg/kg/min).
• Dose up to 15 μg/kg/min increase cardiac contractility without greatly affecting peripheral resistance.
• Vasoconstriction progressively dominates at higher perfusion rates.
• Significantly increases myocardial oxygen consumption. Based on this exercise mimicking behaviour, it is used as a pharmacological stress agent for diagnostic perfusion imaging .
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IsoprenalineIsoprenaline
• Isoprenaline is a potent, relatively pure β-receptor stimulant.
• It has powerful chronotropic and inotropic properties, with potent systemic vasodilator effect.
• Its stimulatory effect on stroke volume is counterbalanced by drop in SVR, which results in a net neutral impact on CO.
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PhenylephrinePhenylephrine
• Phenylephrine is a potent α1 receptor agonist with virtually no affinity for β-receptors.
• It is used primarily as a rapid bolus for immediate correction of sudden severe hypotension.
• It has no direct effect on heart rate, although it can induce significant baroreceptor mediated reflex rate responses after rapid alterations in MAP.
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Adrenoceptor dynamicsAdrenoceptor dynamics
• Desensitisation / down-regulation
• Chronic heart failure
• Prolonged use of inotrope / vasopressor
• Sespis / acidosis
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Other Vasopressors
• Vasopressin• Exogenous form of ADH• Acts on kidney to retain water & on
peripheral blood vessels to cause intense vasoconstriction
• V1 receptors
• Used in severe shock• Used in cardiac arrest in USA
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VasopressinVasopressin
• Vasopressin also known as “antidiuretic hormone” is stored primarily in granules in the posterior pituitary gland and is released in response to osmotic, chemoreceptor and baroreceptor stimuli.
• It exerts its effects through V1 receptor on vascular smooth muscle and oxytocin receptors causing vasoconstriction whereas stimulation of V2 receptors mediates water reabsorption by enhancing renal collecting duct permeability.
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EffectsEffects• vasopressin stimulation tends to cause constriction and
increase in SVR.
• Vasopressin modulated increase in vascular sensitivity to noradrenaline further augments its vasopressor effect.
• Briefly, exogenously administered vasopressin may counteract its relative deficiency which is seen in established sepsis.
• It may also directly influence the mechanisms involved in the pathogenesis of vasodilation through inhibition of ATP-activated K+ channel, attenuation of nitrous oxide production and reversal of adrenergic receptor down regulation.
• Vasopressor effect of vasopressin is not affected by hypoxia and acidosis which commonly develop in shock of any origin.
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Other InotropesOther Inotropes
• cAMP dependent• Phosphodiesterase inhibitors• Glucagon
• cAMP independent• Digoxin• Calcium• levosimendan
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Phosphodiesterase InhibitorsPhosphodiesterase Inhibitors
G - Protein Adenyl cyclase
ATP cAMPIncreased
heart muscle contractility
Adrenaline
AMP
PDE 3
X
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Phosphodiesterase inhibitorsPhosphodiesterase inhibitors• Phosphodiesterase inhibitors (PDI), such as
amrinone and milrinone are non-adrenergic drugs with inotropic and vasodilator actions.
• their effects are similar to those of dobutamine but with a lower incidence of arrhythmias.
• PDI are most often used to treat patients with impaired cardiac function and medically refractory heart failure
• These agents act by inhibiting breakdown of cAMP in cardiac and vascular smooth muscles resulting in increased myocardial contractility and peripheral vascular dilation.
• Milrinone has a longer half-life (2-4 hours) than any other inotropic medications.
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Calcium sensitizing agentsCalcium sensitizing agents
• Calcium sensitizers are a recently developed class of inotropic agents
• Levosimendan is the most well known drug among this class
• It increase calcium binding to contractile proteins and also activates ATP sensitive K+ channels. Calcium dependent binding to contractile protein enhances ventricular contractility without increasing intracellular calcium concentration.
• The opening of K+channel leads to arteriolar and venous vasodilation. The combination of improved contractile performance and vasodilation is particularly beneficial during acute and chronic HF.
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Primary mechanism: In diastole the binding pocket is not exposed.
In systole Ca2+ binds to troponin C and exposes a hydrophobic binding pocket. Levosimendan stabilizes troponin C and prolongs the binding of Ca2+ .
Dual mechanism:Also has ‘anti-ischaemic’ effect via ATP-dependent K+ channel activation in cardiac myocytes.
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Use of Inotropes and Vasopressors in Use of Inotropes and Vasopressors in Various Types of ShockVarious Types of Shock
• Non-cardiogenic shock
• Septic Shock:
• Impaired ventricular function,• Pathological vasodilation,• Deranged micro-vascular flow, • Increased capillary permeability and
hypovolaemia
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Septic ShockSeptic Shock
• Vasopressor and inotropic agents remain the cornerstone for the management of septic shock after fluid administration.
• There is no standard dosing regimen for vasopressor and inotropic agents.
• Human and animal studies suggest some advantage of noradrenaline and dopamine over adrenaline.
• dopamine administration is associated with greater mortality and a higher incidence of arrhythmic events
• noradrenaline is more potent than dopamine and may be more effective at reversing hypotension in septic shock.
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Septic Shock:Septic Shock:
• VASST trial:• A randomized, controlled trial comparing
norepinephrine alone to norepinephrine plus vasopressin at 0.03 units/min,
• patients receiving <15 μg/min norepinephrine at the time of randomization was better with vasopressin.
• dobutamine is the first choice inotropic agent for patients with measured or suspected low cardiac output in the presence of adequate left ventricular filling pressure
• Septic patients who remain hypotensive after fluid resuscitation may have low, normal, or increased cardiac outputs.
• Therefore, treatment with a combined inotrope/vasopressor, such as noradrenaline or dopamine, is recommended if cardiac output is not measured.
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Anaphylactic shockAnaphylactic shock
• The treatment of choice for anaphylaxis is adrenaline.
• The recommended dose is 0.3 to 0.5 mg intramuscularly (IM) every 5 to 10 minutes for adults
• Intravenous epinephrine is reserved for cases of cardiovascular collapse,refractory to IM therapy
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Hemorrhagic shockHemorrhagic shock
• Vasopressors are rarely indicated and should be considered only when volume replacement is complete, haemorrhage is arrested and hypotension continues .
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Cardiogenic shock complicating Cardiogenic shock complicating acute myocardial infarctionacute myocardial infarction
• These agents increase myocardial oxygen consumption.
• However,critical hypotension itself compromises myocardial perfusion, leading to elevated left ventricular (LV) filling pressures, increased myocardial oxygen requirements, and further reduction in the coronary perfusion gradient.
• The lowest possible doses of inotropic and vasopressor agents should be used to adequately support vital tissue perfusion while limiting the adverse effects.
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Cardiogenic shock complicating Cardiogenic shock complicating acute myocardial infarctionacute myocardial infarction
• Dobutamine should be used as a first line agent if systolic blood pressure ranges in between 70-100 mm Hg without signs and symptoms of shock
• In patients with,hypotension along with sign of shock, Dopamine is the preferred agent
• Moderate doses of combination of medications may be more effective than maximal doses of any individual medication.
• In patients with systolic blood pressure <70 mm Hg and sign/symptoms suggestive of shock, use of noradrenaline is recommended
• Vasopressin therapy may thus be effective in norepinephrine resistant shock
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Cardiogenic shock complicating Cardiogenic shock complicating acute myocardial infarctionacute myocardial infarction
• During early cardiogenic shock, endogenous vasopressin levels are increased significantly to maintain end organ perfusion.
• As the shock continues, falling plasma vasopressin level contributes to a loss of vascular tone and worsening hypotension.
• Vasopressin therapy may thus be effective in norepinephrine resistant shock.
• this agent increase MAP without adversely impacting cardiac index and wedge pressure.
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Congestive heart failureCongestive heart failure• Inotropic therapy is used in the management of
decompensated heart failure to lower end-diastolic pressure and improve dieresis.
• The most commonly recommended initial inotropic therapies (dobutamine, dopamine and milrinone) for refractory HF are used to improve cardiac output, enhance diuresis by improving renal perfusion and decreasing SVR.
• use of levosimendan is significantly associated with improved symptoms but not survival.
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Cardiopulmonary arrestCardiopulmonary arrest
• Inotropic and vasopressor agents are a mainstay of resuscitation therapy during cardiopulmonary arrest.
• Epinephrine, with its potent vasopressor and inotropic properties, can rapidly increase diastolic blood pressure to facilitate coronary perfusion and help restore organised myocardial contractility.
• The current AHA guideline have incorporated vasopressin (single bolus of 40 U) as a one-time alternative to the first or second dose of adrenaline with pulse-less electrical activity or asystole and for pulse-less ventricular tachycardia or ventricular fibrillation
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That’s AllThat’s All
Thank YouThank You