Cardiac Anesthesia Flashcards
(36 cards)
Important things to know about protamine:
1- a polycationic protein used to neutralize heparin
2- 1 mg protamine : 100 U heparin
3- measure ACT 3 minutes after protamine administration
4- associated with a spectrum of hemodynamic effects
5- Most devastating complication: profound pulmonary hypertension accompanied by elevated CVP, flaccid distended RV, and systemic hypotension.
6- Heparin-protamine complex is removed by the reticuloendothelial system.
Why do we administer cardiovascular drugs?
Cardiovascular drugs allow us to pharmacologically modify all of the components of organ perfusion, including:
1- preload (end-diastolic volume) 2- afterload 3- inotropy 4- heart rate 5- myocardial oxygen supply and demand
In layman’s terms, describe the Frank-Starling principle.
Increased myocardial fiber length (i.e., end-diastolic volume) improves contractility up to a point of optimal contractile state, further stretching results in declining performance.
Discuss the limitations of drugs that alter vascular tone.
Preload can be altered with intravascular volume shifts and with drugs that change vascular tone, most notably the venous capacitance vessels.
Arterial vasodilators may shift failing myocardium to a more effective contractile state as a result of afterload reduction and decreased impedance to ventricular ejection.
The intrinsic contractile state is not improved by vasodilators, in contrast to the effect of positive inotropic agents.
What is the goal of inotropic support?
To optimize end-organ perfusion by increasing myocardial contractility and thus improve cardiac output.
Discuss the hemodynamic profile of the phosphodiesterase III inhibitors amrinone and milrinone.
Amrinone and milrinone are approximately equipotent to dopamine and dobutamine in increasing cardiac output through increased inotropy and improved lusitropy (myocardial relaxation).
What is the mechanism of action of amrinone and milrinone?
They are phosphodiesterase III inhibitors, which lead to a decrease in the breakdown of cAMP.
The resultant increase in cAMP will increase the heart’s contractility and decrease afterload through vasodilation.
What adverse effects can result from use of phosphodiesterase inhibitors? How are these minimized?
Because the vasodilator effects may be profound, concurrent use of vasoconstrictors (e.g., epinephrine, norepinephrine, and phenylephrine) is often necessary, particularly after CPB.
Prolonged infusion of amrinone, but not milrinone, may cause significant thrombocytopenia through nonimmune-mediated peripheral platelet destruction.
How does increasing intracellular cAMP affect the cardiac myocyte?
Increased intracellular cAMP leads to elevated intracellular calcium, increased contractility, and improved lusitropy (myocardial relaxation). The end result is a restoration of the myofilaments to their resting state.
Describe hemodynamic profile of epinephrine.
Epinephrine has potent vasoconstrictive effects and ability to increase cardiac output.
Low dose: 0.12 mcg/kg/min, primarily alpha stimulation
Describe the hemodynamic profile of norepinephrine.
The potency of norepinephrine in stimulating b-adrenergic receptors is similar to that of
epinephrine, but it results in significant a-adrenergic stimulation at much lower doses. Typical dosage ranges are 0.02 to 0.25 mcg/kg/min
Describe the hemodynamic profile of dopamine.
Dopamine stimulates specific postjunctional dopaminergic receptors in renal, mesenteric, and coronary arterial beds to produce vasodilation. These dopaminergic effects occur at lower doses (0.5 to 1.0 mcg/kg/min), becoming maximal at 2 to 3 mcg/kg/min.
At intermediate doses (2 to 6 mcg/kg/min) b1-adrenergic stimulation is evident. (This is the dose used in the ACLS bradycardia protocol.)
Beginning at doses of about 10 mcg/kg/min (but as low as 5 mcg/kg/min), a-adrenergic stimulation is seen, which at higher doses overcomes dopaminergic effects, producing vasoconstriction.
Describe hemodynamic profile of isoproterenol.
Isoproterenol is an extremely potent b1- and b2- agonist that possesses no alpha-stimulating
properties. It increases heart rate, automaticity, and contractility and dilates both venous capacitance and arterial vessels. It may be a good choice for heart-rate maintenance in a denervated nonpaced transplanted heart.
Describe hemodynamic profile of dobutamine.
Dobutamine acts principally on b-adrenergic receptors, impacting b1-receptors in a relatively selective fashion. In addition, it has a mild indirect b1-stimulating effect that is secondary to
prevention of norepinephrine reuptake but is offset by slightly more potent b2-stimulation.
Generally at clinical doses minimal increases in heart rate, positive inotropy, increased cardiac output, and minimal or modest decreases in SVR and PVR occur. Because of the indirect b1-stimulating effect, patients concurrently
receiving b-blockers can exhibit marked increases in systemic vascular resistance without improvement in cardiac output. In addition, an occasional patient will display dose-related increases in heart rate.
Which characteristics of b-adrenergic agonists limit their effectiveness?
Positive chronotropic and arrhythmogenic effects (dose-dependent effect with epinephrine, isoproterenol, and dobutamine) result in increased myocardial oxygen consumption.
Vasoconstriction secondary to a1-activation (with norepinephrine, high-dose epinephrine,
and high-dose dopamine) results in increased afterload and subsequent increased
myocardial wall tension.
Isoproterenol and dobutamine to a lesser extent produce vasodilation caused by stimulation of vascular b2-receptors. Excessive vasodilation may decrease coronary perfusion.
How may the side effects and limitations of b-adrenergic agonists be minimized?
Side effects may be decreased by appropriate dosage adjustments and use of combinations of agents.
What are the mechanism and sites of action of nitrovasodilators?
Nitrates (ie nitroglycerin and sodium nitroprusside) are pro-drugs that penetrate the vascular endothelium and become reduced to nitric oxide (NO).
Nitroglycerin requires intact endothelial enzymatic activity, which is not present in the smallest or damaged vessels, whereas nitroprusside nonenzymatically degrades into NO and cyanide. NO then stimulates production of cyclic guanosine monophosphate (cGMP), resulting in decreased cellular calcium levels and thus vascular smooth muscle relaxation.
Sodium nitroprusside acts primarily on the arterial vasculature whereas nitroglycerin has its
most prominent effect on venous capacitance vessels.
NO can also be delivered directly to the pulmonary circulation by inhalation, thereby reaching the pulmonary vascular smooth muscle by diffusion across the alveolar-capillary membrane. Direct delivery to the pulmonary circulation reduces potentially undesirable systemic hypotension and causes specific pulmonary vasodilation.
What is fenoldopam?
A potent short-acting dopamine-1 agonist that decreases SVR and increase renal blood flow via DA-1 receptor-mediated vasodilation.
Increases renal cortical and outer medullary blood flow.
T or F: ARF is a frequent complication of cardiac surgery, with a reported incidence of 30-50% in more complicated procedures.
True
T or F: The current evidence-based opinion is that dopamine does not prevent ARF and should not be used for this purpose, and the use of dopamine may be harmful by causing tachycardia and MI due to its adrenergic effects.
True
Describe the mechanism of action of labetalol. What is the onset and duration of action?
Mechanism of action: alpha and beta blocker
Onset: 2-5 minutes
Duration of action: 2-4 hours
Describe the mechanism of action of esmolol. What is the onset and duration of action?
Mechanism of action: ultra-short acting beta blocker
Onset: 60 seconds
Duration of action: 10-20 minutes
Describe the mechanism of action of nicardipine. What is the onset and duration of action?
Mechanism of action: calcium channel blocker
Onset: 5-15 minutes
Duration of action: 4-6 hours
Describe the mechanism of action of nitroprusside. What is the onset and duration of action?
Mechanism of action: arterial and venous vasodilator
Onset: within seconds
Duration of action: 1-2 minutes
Can result in cyanide toxicity
