Positive Inotropes and Vasopressors Flashcards
Positive inotrope
increases strength of heart muscle contraction
Vasopressors
increase blood pressure by contracting blood vessels
Beta 1 receptors
1.) increase HR and contractility
2.) release renin for the RAAS system and increase sodium and water retention
Beta 2 receptors
Dilate smooth muscle cells, bronchodilation, decrease gut motility, secrete aqueous humor, increase glucose, and release glucagon
Alpha 1 receptors
Constrict the walls of blood vessels, cause pupil dilation (mydriasis), and urinary retention
Alpha 2 receptors
Negative feedback loop which limits pre-synaptic NT release
Ejection fraction
percentage of end-diastolic volume ejected with each contraction (SV/end diastolic volume)
Afterload
the force resisting myocardial fiber contraction at the start of systole. Arterial vasodilation lowers after load
Frank starling mechanism of the heart
If venous return is increased, the ventricular end diastolic pressure and volume of the ventricle are increased, which stretches the sarcomeres (increases preload) this increased SV because of increased contraction
Diastolic disfunction
Impaired ventricular filling. Primary abnormality in HF with preserved ejection fraction. Lower EDV = lower CO (hypertrophy heart)
Systolic disfunction
impaired ventricular emptying, loss of contractile strength. Abnormality seen in HF with reduced EF. Increased ESV = decreased CO
Inotropes
Beta agonists which increased contractility
Vasopressors
Alpha 1 agonists which increase SVR
Dobutamine
Beta agonist. Highly selective for Beta 1. Increased cAMP –> increased PKA –> Increase Ca2+ –> increase force of contraction and increase O2 and energy demand. Also some Beta 2 activity. Vasodilator vessels and lowers peripheral vascular resistance. NOT APPROPRIATE FOR CHRONIC HF. Tachyphylaxis (tolerance) SE: tachycardia, palpitations, and arrhythmias
Milrinone
Phosphodiesterase inhibitor. Decreases the breakdown of cAMP. Leads to increase force of contraction and smooth muscle vasodilation (Inodilator). Strong vasodilator because it doesn’t bind to receptors but work intracellularly. SHOULD NOT BE USED FOR CHRONIC HF. SE: arrhythmias and hypotension
Dopamine
Action dependent on dose. Uses: severe hypotension, acute HF, shock (vasodilatory, cardiogenic), and severe bradycardia. Adverse effects: tachycardia, dysrhythmias, N&V, and ischemia of digits and various organ systems
Low dose dopamine (<3mcg/kg/min)
Stimulates renal dopamine receptors. Vasodilation (increases renal blood flow) and increased natriuresis (increased Na elimination)
Moderate dose dopamine (4-10 mcg/kg/min)
Primary action Beta 1 receptors. Increase cAMP –> increase intracellular Ca2+ –> increased contractility and HR –> Increased CO
High dose dopamine (>10mcg/kg/min)
Primary action is on alpha 1 receptors. Increase in vascular intracellular Ca2+ –> vasoconstriction –> increased SVR –> increased blood pressure
Vasopressors: epinephrine
Balanced B1, B2, and A1 adrenergic agonist. Increased contractility, HR, and SVR
Vasopressor: phenylephrine
Potent A1 agonist. (No beta). Increases SVR
Digoxin
Blocks Na-K ATPase which prevents Na from leaving the cell which blocks the Na-Ca exchanger and increases intracellular calcium. Used for atrial fib/flutter and HF with reduced EF. Narrow therapeutic window (0.5-2.0 ng/ml)
Vasopressor: Norepinephrine
Potent A1 and modest B stimulation (1>2). A1 = vasoconstriction (increased SVR increased BP) and B = Increased CO but HR is mostly unchanged.
