Cardiac Drugs Flashcards
Cardiac Glycosides (Digoxin) MOA & Use
Digoxin
MOA: increase contractility of the heart and prolongs AV refractory period
-Increase in calcium in the SR
Clinical use: inotrope (increases contractility), anti-arrhythmic agent for SVT, AVNRTs
Dopamine
MOA & Use
Dopamine
MOA: beta 1 receptor agonist
-Increase cAMP in cell to cause increased Ca+ to increase contractility and HR
-Also acts on B2 and A1
Clinical use:
-2-10mcg/kg/min will stimulate B1 and cause inotropy
->10mcg/kg/min will cause A1 activation and increased SVR
-Short term use
-Bradycardia
Dobutamine
MOA & Use
Dobutamine
MOA: B1 receptor agonist with minimal effects on SVR
Clinical use: cardiogenic shock
*Be careful because an increase in CO can cause reflex vasodilation which can decompensate patients in cardiogenic shock
Norepinephrine
MOA & Use
Norepinephrine
MOA: primarily A1 agonist with some B1 activity to increase HR and contractility
Clinical uses: distributive shock, hemorrhagic shock
Note: primarily a chronotrope in that it mainly increases SVR before CO
Epinephrine
MOA & Use
Epinephrine
MOA: primarily affects A1 but also works on B2 and B1 receptors to increase inotropy (at low doses)
Clinical use: cardiac arrest, distributive shock
-Inotropy and chronotropy work together to raise BP
-Bradycardia
Vasopressin
MOA & Use
Vasopressin
MOA: potent non-adrenergic vasoconstrictor when administered IV
Clinical use: sepsis, advanced cardiac arrest support
Angiotensin Receptor Blocker
MOA & Use
Angiotensin Receptor Blockers (“-sartans”)
MOA: competitively inhibit binding of AT2 to its receptor, thereby down regulating AT1 and preventing vasoconstriction, sympathetic activation and aldosterone
Clinical uses: HTN, CHF
Calcium Channel Blockers
MOA & Use
Calcium Channel Blockers
MOA: inhibits Ca+ entry through L-type Ca+ channels into myocardium and vascular smooth muscle myocytes, decrease contractility (negative inotrope), decreases vasoconstriction, suppresses AV node conduction
Clinical uses: HTN, angina (negative inotrope and vasodilation get more O2 into CAs), SVT (slow AV node conduction)
Organic Nitrates
MOA & Use
Organic Nitrates
MOA: converted NO to cause relaxation of vascular smooth muscle
Clinical use: angina (through preload reduction which lowers stress and O2 consumption of myocardium), prinzmetal angina, acute heart failure
Note: at low doses, produces more venous dilation than arterial dilation; at high doses cause arterial dilation and possibly reflex tachycardia
Peripheral A1 Receptor Antagonists
MOA & Use
Peripheral A1 Receptor Antagonists
MOA: if A1 selective they will decrease SVR, if they also act on presynaptic A2, they can prevent negative feedback inhibition on A2 causing norepinephrine to be released
Clinical use: HTN
Note: not used anymore
Beta Blockers
MOA & Use
Beta Blockers ("-olol")
MOA: negative inotropy, chronotropy and decreased AV node conduction
Clinical use: IHD (decrease myocardial O2 demand), HTN (decrease CO), heart failure (even though this seems counterintuitive; BB protect failing heart against large amounts of circulating catecholamines)
Note: bronchospasm is a relative contraindication, can case conduction blocks, abrupt withdrawal can exacerbate ischemia
Class I: Na Channel Blockers
MOA & Use
Na Channel Blockers ex. Lidocaine
MOA: block fast Na channels responsible for phase 0, depolarization of the action potential in Purkinje fibres
Clinical use: A Fib., A. Flutter, SVT, VT
Class II: Beta Blockers
MOA & Use
Beta Blockers
MOA: lengthen refractory period of AV Node, lengthen phase 4 of the action potential
Clinical use: SVT, VT
Class III: K Channel Blockers
MOA & Use
K Channel Blockers ex. Amiodarone
MOA: prolong action potential duration
Clinical use: VT, SVT, V Fib. (acutely), Suppression of A. Fib. and A. Flutter long term
Note: can cause Torsades des pointes
Ca Channel Blockers
MOA & Use
Ca Channel Blockers
MOA: block L-type cardiac Ca channels to block AV node conduction, stretch out phase 0 of the action potential
Clinical use: SVT
