Making up for lost time
Been there, done that
My side drugs
Side drugs bring baggage
Anything & Everything
100
A compensatory mechanism in CHF
1. Neurohormonal Systems (SNS, RAAS, endothelin-1, arginine vasopressin, natriuretic peptides)
2. Ventricular Dilation
3. Ventricular Hypertrophy and Remodeling
100
Because of aldosterone's effect on bradykinin, ACE inhibitors have this side effect that is not seen in ARBs.
What is dry cough?
ACE degrades bradykinin which in high concentrations can cause cough.
ACE inhibitors (C = cough)
ARBs inhibit angiotensin II from binding to its receptors (so they have no effect on ACE)
100
This inotropic agent works by inhibiting the Na/K pump and increasing intracellular calcium concentration.
What is digoxin?
100
This class(es) of drugs are not to be used with dopamine and dobutamine.
What are beta blockers and alpha blockers?
Dopamine and dobutamine = beta agonists
Beta blockers and alpha blockers blunt the effect of beta agonists.
100
This class of drugs is important for restoring fluid balance.
What is: diuretics, ACE-I, natriuretic peptide?
Decrease preload
High preload → Pressure overload → hypertrophy → ischemia
200
Long-term release of NE and Epi from SNS will cause increased SVR and prolonged tachycardia resulting in decreased CO through these 2 mechanisms.
What is increased afterload and decreased diastolic filling time?
CO = SV x HR
200
Because of its effect on HR, this class of drugs is contraindicated in patients with symptomatic bradycardia.
What is beta-blockers?
Beta 1 receptors (in heart): increased HR and contractility
Only use the ones that decrease mortality:
carvedilol, metoprolol, bisoprolol, (nebivolol, labetalol)
200
This beta agonist activates different adrenergic receptors depending on its dosage.
What is dopamine?
1-5 mcg/kg/min: DA1 receptor (renal vasodilation)
5-15 mcg/kg/min: b1 receptor (increased contractility)
>15 mcg/kg/min: a1 receptor (vasoconstriction of vessels)
200
This characteristic of digoxin explains its high risk for toxicity.
What is narrow therapeutic index?
Toxicity → visual disturbances, confusion, nausea, vomiting, anorexia
Other AE → PVCs, tachycardia, bradycardia, arrhythmias, heart block
200
Digoxin's parasympathomimetic activity which slows AV nodal conduction velocity and increases AV nodal refractory period protects against what.
What is arrhythmias?
300
Angiotensin II has this major effect on peripheral blood vessels
What is vasoconstriction?
Other Effects:
- norepinephrine release
- endothelin-1 and AVP release
- ventricular hypertrophy and remodeling
- stimulates apoptosis
- vasoconstriction of efferent renal arteriole (maintains renal perfusion pressure)
300
Nitroglycerin and nitroprusside are converted into nitric oxide and increase cellular cGMP levels resulting in this major effect on blood vessels.
What is venous vasodilation?
Nitrates → decrease preload
Nitroglycerin - decreases myocardial O2 demand; no effect on CO
Nitroprusside - decreases O2 demand, decreases SVR; increases CO
300
Milrinone, a PDE inhibitor, increases Ca2+ which has what effects on the heart?
What is positive inotropy?
- Increases contractility → increases CO
300
Milrinone's vasodilating effects in the blood vessels results in an increased risk for this side effect.
PDE inhibitor
What is hypotension?
Other AE:
- ventricular arrhythmias
- angina
- reversible thrombocytopenia
300
Drugs that block P-glycoprotein (PGP) will affect the absorption, bioavailability, and elimination of this drug.
What is digoxin?
Digoxin has narrow TI; toxicity risk is high
400
When BNP (B-type natriuretic peptide) is released from the left ventricle, it inhibits SNS and RAAS by decreasing the release of these 2 hormones.
What is aldosterone and norepinephrine?
Natriuretic peptides BALANCE the long-term effects of RAAS and SNS. Eventual down-regulation of ANP/BNP receptors result in takeover by RAAS/other neurohormones.
- inhibit Na+ and H2O reabsorption → decreased preload
- Peripheral and coronary VD → decreased preload
400
Spironolactone and eplerenone are a part of this drug class, which is contraindicated in patients already taking ACE inhibitors and ARBs.
What is aldosterone receptor antagonists?
ARAs: inhibits the effects of aldosterone
Other contraindications:
- high Potassium
- renal dysfunction (increased SCr)
- Use of other potent CYP3A4 inhibitors (eplerenone)
400
Nesiritide is an exogenous form of this hormone, synthesized by recombinant DNA.
What is BNP (B-type natriuretic peptide)?
Increases cGMP → smooth muscle relaxation → vasodilation (decreased SVR → increased CO)
BALANCES the effects on neurohormonal systems
400
This dose-limiting side effect of nesiritide may be due to its inhibitory effects on the RAAS and SNS pathways.
What is hypotension?
Decrease norepinephrine and aldosterone release
Increases cGMP → arterial and venous vasodilation → Decreases preload
Contraindicated if SBP < 90
500
Prolonged release of aldosterone will increase myocardial fibrosis which can lead to this common finding in CHF.
What is arrhythmias?
Fibrosis impairs mechano-electric coupling between myocytes and reduces cardiac contraction → increasing risk of arrhythmogenesis.
500
Mrs. Miller received furosemide, nitroglycerin, lisinopril, and carvedilol. Which of these will decrease her Na+ retention?
What is furosemide and lisinopril?
furosemide - loop diuretic (-mide)
nitroglycerin - nitrate (nitro-)
lisinopril - ACE inhibitor (-pril)
carvedilol - beta blocker (-lol)
500
Dobutamine acts on a1, b1, and b2 receptors. However, it acts predominantly on this receptor to have this effect.
What is b1 and what is increased contractility?
Increased contractility → Increased SV → increased CO
(increased HR at higher doses)
500
Unlike milrinone (PDEI) and nesiritide (BNP), use of beta agonists dopamine and dobutamine, results in this effect on blood pressure.
What is hypertension?
a1 receptors → vasoconstriction → increased SVR