Term
| 2017 recommendations for HF? All classes + Class I, IIa |
|
Definition
|
|
Term
| 2016 european HF recommendation |
|
Definition
|
|
Term
|
Definition
|
|
Term
| ACEI and ARB effect on RAAS and MOA diagram |
|
Definition
|
|
Term
|
Definition
• Blocks Angiotensin Converting Anzyme (ACE)
• Prevents conversion of angiotensin I to angiotensin II
• Decreases angiotensin II mediated vasoconstriction
• Decreases afterload; lowers blood pressure |
|
|
Term
|
Definition
| Captopril (Capoten), Enalapril (Vasotec), Lisinopril (Zestril), Ramipril (Altace), Trandolapril (Mavik) |
|
|
Term
| ARB MOA and place in therapy |
|
Definition
• Selectively blocks angiotensin II from binding AT1 receptor
• Decreases angiotensin II mediated vasoconstriction
• Decreases afterload; lowers blood pressure
• Place in therapy
• Intolerant of ACEIs or ARNIs |
|
|
Term
|
Definition
| Candesartan (Atacand), Losartan (Cozaar), Valsartan (Diovan) |
|
|
Term
ADEs
• First dose hypotension
• Hyperkalemia
• Acute kidney injury- Actually thought to be renoprotective
• Cough ~10%- Anytime on therapy; ACEI >> ARB
• Angioedema ~0.1–0.5%- Within days of initiation; greater risk in African-Americans |
|
Definition
ACEI/ARB
ACEI Captopril (Capoten), Enalapril (Vasotec), Lisinopril (Zestril), Ramipril (Altace), Trandolapril (Mavik)
ARB Candesartan (Atacand), Losartan (Cozaar), Valsartan (Diovan) |
|
|
Term
| Sacubitril/Valsartan MOA Diagram RAAS, NPS, affects |
|
Definition
|
|
Term
|
Definition
| Pts on Sacubitril/Valsartan lived 2 years longer and had fewer adverse effects. |
|
|
Term
| One side effect to worry about w Sacubitril/Valsartan |
|
Definition
|
|
Term
| Contraindications to Sacubitril/Valsartan |
|
Definition
• History of angioedema to ACEI/ARB
• Concomitant ACEI use within 36 hours |
|
|
Term
| MRAs, Metabolic corticoid antagonists MOA diagram |
|
Definition
|
|
Term
| MRA Metabolic corticoid antagonists agents |
|
Definition
| Eplerenone (Inspra), Spironolactone (Aldactone) |
|
|
Term
| MRA Metabolic corticoid antagonists MOA |
|
Definition
| • Block aldosterone-mediated Na/K antiporter activity in collecting duct |
|
|
Term
ADE
Hyperkalemia, gynecomastia |
|
Definition
MRA Metabolic corticoid antagonists
• Hyperkalemia, gynecomastia (spironolactone)
Eplerenone (Inspra), Spironolactone (Aldactone) |
|
|
Term
| Beta blockers indications |
|
Definition
| Hypertension,AMI(within24hoursofhospital admission and at discharge), angina pectoris (stable), arrhythmias |
|
|
Term
| Beta blockers contraindications |
|
Definition
| Allergy,cardiogenicshock,severeheartfailure, bradycardia, second- or third-degree heart block |
|
|
Term
| has SEs Bradycardia, AV nodal block, hypotension, dizziness, bronchospasm, fatigue, depressed mood |
|
Definition
Beta blockers
Bisoprolol (Zabeta), Carvedilol (Coreg), Motoprolol succinate (Toprol XL), Nebivolol (Bystolic) |
|
|
Term
| Beta blocker agents for HF |
|
Definition
| Bisoprolol (Zabeta), Carvedilol (Coreg), Motoprolol succinate (Toprol XL), Nebivolol (Bystolic) |
|
|
Term
| Funny Channel inhibitor agent |
|
Definition
|
|
Term
|
Definition
| It works only by delaying conduction of sodium and potassium across what is called the IF channel, or the funny channel. Only works at SA node (useful for sinus rhythm but not aberrant conductin pathways) |
|
|
Term
| ADEs HF, Symptomatic Bradycardia, Asymptomatic Bradycardia, Atrial Fibrillaiton, Phosphenes |
|
Definition
| Ivabradine, funny channel inhibitor, IF channel |
|
|
Term
| Ivabradine place in therapy |
|
Definition
| • Resting HR > 70 bpm despite max tolerated β- blockade |
|
|
Term
| Ivabradine contraindicaxtion |
|
Definition
Contraindications
• Acute decompensated heart failure
• BP<90/50mmHg
• SSS, SA block, or 3o AV block
• Strong CYP3A4 inhibitors |
|
|
Term
|
Definition
| Isosorbide Dinitrate/Hydralazine, Nitroglycerin (component of Isosorbide Dinitrate/Hydralazine), Nitroprusside, Nesiritide |
|
|
Term
| Isosorbide Dinitrate/ Hydralazine MOA |
|
Definition
• Direct vasodilatory combination
• Isosorbide relaxes venules > arterioles • Hydralazine relaxes arterioles |
|
|
Term
| Isosorbide Dinitrate/Hydralazine place in therapy |
|
Definition
| • Mortality benefit only in African-American HFrEF |
|
|
Term
has SEs
• Hypotension, headache, weakness
• Chest pain |
|
Definition
| Isosorbide Dinitrate/Hydralazine |
|
|
Term
| Nitroglycerin MOA and Indication |
|
Definition
(component of isosorbide dinitrate/hydralazine)
• Venodilator
• Reduce preload and ventricular stretch
• Rapid relief of pulmonary congestion
• Ideal for HF with HTN, ACS, or significant mitral regurgitation |
|
|
Term
Has SEs of
• Postural hypotension
• Tachycardia
• Headache
• Tachyphylaxis develops within 24 hours
• DDI - Sildenafil (Viagra, Revatio), Tadalafil (Cialis), Vardenafil (Levitra) (PDEI)- Hypotension |
|
Definition
|
|
Term
| Nitroprusside MOA and monitoring |
|
Definition
• Mixed arterial/venodilator
• Reduce preload and afterload
• Invasive arterial monitoring typically required |
|
|
Term
Has SEs
• Excessive hypotension, especially HFpEF due to volume sensitivity
• Thiocyanate/cyanide toxicity |
|
Definition
|
|
Term
|
Definition
• RecombinantBNP
• Increases cAMP-veno and arteriolar vasodilitation
• Naturesis |
|
|
Term
has SEs
• Hypotension, headache, nausea
• Renal toxicity and death
• Injection site extravasation |
|
Definition
|
|
Term
| loop diuretic MOA diagram |
|
Definition
|
|
Term
| Loop diuretic for HF agents |
|
Definition
| furosemide(Lasix®) (most common),bumetanide (Bumex®), torsemide (Demadex®), ethacrynic acid (Edecrin®)(no sulfonamide) |
|
|
Term
|
Definition
| • Inhibit Na/K/2Cl symporter on thick ascending limb of the loop of Henle |
|
|
Term
has adverse effects of
• Hypokalemia, hypomagnesemia
• Cramping
• Hypotension
• Hearing decrements |
|
Definition
Loop diuretics
furosemide(Lasix®),bumetanide (Bumex®), torsemide (Demadex®), ethacrynic acid (Edecrin®) |
|
|
Term
|
Definition
| Dopamine, Dobutamine, Milrinone |
|
|
Term
|
Definition
• Mixed alpha and beta agonist
• Dopamine-arterial dilator, especially kidney
• β1-inotropy, arrhythmogenicity
• α-vasoconstriction |
|
|
Term
Has SE
• Tachyarrhythmias
• Hypertension
• Extravasation necrosis |
|
Definition
|
|
Term
|
Definition
• Beta agonist
• β1-inotropy, arrhythmogenicity
• β2 -peripheral vasodilation |
|
|
Term
Has SEs
• Tachyarrhythmias
• Hypertension
• Hypotension
• Angina |
|
Definition
|
|
Term
|
Definition
• Phosphodiesterase-3i nhibitor
• Increase intracellular Ca++
• Vasodilation
• Inotropy |
|
|
Term
has SEs
• Arrhythmias
• Hypotension
• Headache |
|
Definition
|
|
Term
| digoxin and potassium relationship |
|
Definition
So as we mentioned that digoxin is influenced by the binding site of potassium, under circumstances of low circulating potassium or hypokalemia, we have more unoccupied receptors, therefore more places for digoxin to bind. So we can have increased physiologic effects of digoxin and many, many side effects under circumstances of hypokalemia.
However, when patients have the opposite problem, or they have hyperkalemia, digoxin may not be as effective as we thought it should be. In fact, actually hyperkalemia may be a sensitive sign for digoxin toxicity, because digoxin has outpaced all of the available potassium on the sodium potassium ATPase pumps. So high resting potassium in a patient who is on chronic digoxin or acute digoxin therapy may actually be a signal of toxicity |
|
|
Term
| digoxin and parasympathetic innervation |
|
Definition
| Now in the neuron, the sodium potassium ATPase pump controls parasympathetic innervation in the vagel nerve. So when potassium is out-competed by digoxin centrally, it actually results in longer parasympathetic innervation at the side of the AV node, which will lower heart rate. So it's a unique mechanism of action, because it makes the heart pump harder, but may also make the heart pump slower, particularly at high concentrations needed to penetrate the blood-brain barrier. |
|
|
Term
|
Definition
1. 3Na+/2K+ ATPase pump inhibitor
• Competes for K+ binding site • Intracellular Na+ increases
2. 3Na+/Ca2+exchanger
• Removes excess Na+
• Intracellular Ca2+ increases
Tn-C
3. Sarcoplasmicreticulum
• High Ca2+ activates troponin-C • Increases cardiac contractility
[image] |
|
|
Term
|
Definition
| Now, I mentioned that the digoxin increases contractility of the heart. But unique and different from all the other inotropes we discussed is it's actual ability to lower heart rate. Now, in the cardiac myocardium is not the only place where sodium ATPas is to be expressed. In fact, this channel was actually discovered in the neurons of shrimp, and it won the investigator a Nobel Prize for doing so in chemistry. |
|
|
Term
Has Adverse effects
Digestive (most common)
Nausea, vomiting, anorexia, diarrhea
Neurologic
Headache, fatigue, disorientation, delirium, confusion
Visual
Blurred vision, altered color perception, greenish-yellow halo
Cardiac
Bradyarrhythmia, heart block, ventricular dysrhythmias |
|
Definition
|
|
Term
| acute vs chronic toxicity of digoxin chart |
|
Definition
|
|
Term
|
Definition
• Symptomatic HF despite GDMT guideline-directed medical therapy
• No mortality benefit
• Lowers rehospitalization only
• Concurrent atrial fibrillation |
|
|
Term
|
Definition
• Human relaxin-2, vascular hormone
• Responsible for many of the hemodynamic adaptions during pregnancy
• Promotes angiogenesis at ischemic sites
• Anti-inflammatory and antifibrotic properties
• t1/2 < 10 min
• Reduces SVR and PCWP
[image] |
|
|
Term
| Omecamtiv Mecarbil MOA, effects |
|
Definition
• Cardiac myosin activator
• Increases entry rate of myosin into the tightly- bound, force-producing state with actin
• No increase in myocardial oxygen demand
• Increased systole/decreased diastolic may impact on coronary perfusion
• Benign troponin leak
[image] |
|
|
Term
| SGLT-2 Inhibitor MOA diagram |
|
Definition
|
|
Term
| HF risk factor management |
|
Definition
|
|
Term
|
Definition
• S = sodium and other dietary restrictions
• C = care in the community
• A = activity
• L = Lasix and other medications
• E = every day weight and symptom monitoring
• S = smoking cessation |
|
|
