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101 Cards in this Set
- Front
- Back
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Which drug classes are used to treat chronic heart failure?
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Vasodilators (ACEI’s, ARB’s, Nitrates, Hydralazine, Alpha-1 Blockers)
Diuretics K+ Sparing Diuretics Digoxin BB’s CCB’s (DHP) Antiarrhythmics Anticoagulants |
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ACE inhibitors and ARBs are recommended for use in ALL Heart Failure patients unless contraindicated.
What are the 6 contraindications |
Cough (for ACEI only)
Angioedema Hyperkalemia (K+ > 5.5) Renal artery stenosis Pregnancy SBP <90 |
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Sodium Nitroprusside (Nipride)
What is MOA? |
Nitric oxide-induced stimulation of guanylate cyclase to convert guanosine triphosphate to cGMP
FYI: In the bloodstream sodium nitroprusside decomposes to release nitric oxide (NO), which causes relaxation of vascular smooth muscle. In the human heart, nitric oxide reduces both total peripheral resistance as well as venous return, thus decreasing both preload and afterload. |
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Nitroglycerin
What is MOA? |
Combines w/sulfhydryl groups in vascular endothelium to create compounds which mimic nitric oxide’s stimulation of guanylate cyclase & production of cGMP
Nitric Oxide is a natural vasodilator! |
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Nesiritide (Natrecor)
What is MOA? |
Recombinant b-type natriuretic peptide binds to natriuretic receptor to stimulate guanylate cyclase and production of cGMP; Vasodilator
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Dobutamine (Dobutrex)
What is MOA? |
Stimulates adenylate cyclase to convert ATP to cAMP-->Increases CO; Minimal peripheral vasodilation
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Milrinone (Primacor)
What is MOA? |
PDE Inhibitor; Inhibits cAMP breakdown in heart -->Increases CO & decreases SVR in vascular smooth muscle
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Aspirin
What is MOA |
Irreversibly inactivates platelet
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Clopidogrel (Plavix)
What is MOA? |
Inhibits ADP receptors, preventing fibrinogen binding at that site & decreasing platelet adhesion & aggregation
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Ticlopidine (Ticlid)
What is MOA? |
Inhibits ADP-induced platelet aggregation
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Isosorbide
What is MOA? |
Stimulates cGMP-->Smooth muscle relaxation of arterial & venous vasculature, decreasing preload & afterload, decreasing CO by decreasing SVR & LV pressure
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Abciximab (ReoPro)
What is MOA? |
Blocks glycoprotein IIb/IIIa receptor site which is binding site for fibrinogen and Factor VIII; reversibly blocks platelet aggregation
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Eptifibatide (Integrilin)
What is MOA? |
Blocks glycoprotein IIb/IIIa receptor site which is binding site for fibrinogen and Factor VIII; reversibly blocks platelet aggregation
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Tirofiban(Aggrastat)
What is MOA? |
Blocks glycoprotein IIb/IIIa receptor site which is binding site for fibrinogen and Factor VIII; reversibly blocks platelet aggregation
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Bivalirudin (Angiomax)
What is MOA? |
Direct thrombin inhibitor
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Digoxin (Lanoxin)
What is MOA? |
Inhibits Na-K+ ATPase -->Increases intracellular Na concentration -->Increased intracellular Ca concentration -->Positive inotropic effect, decreased sympathetic response & decreased renin-angiotensin system output
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Name the 8 drug classifications mentioned to treat chronic heart failure.
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*Vasodilators (ACEI’s, ARB’s, Nitrates, Hydralazine, Alpha-1 Blockers)
*Diuretics *K+ Sparing Diuretics *Digoxin *BB’s *CCB’s—DHP’s *Antiarrhythmics *Anticoagulants |
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What type of vasodilators would be indicated for treatment of chronic heart failure? Why?
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ACE inhibitors and ARBs
recommended in all heart failure patients unless contraindicated. Remember they are used to inhibit the effects of angiotensin II/ block the receptor and thus "Inhibit Vasoconstriction" Nitrates and Hydralazine 2nd line of defense for left ventricular systolic dysfunction or if unable to take ACEI/ ARB Nitrates like nitroglycerine produce rapid symptomatic relief. Hydralazine relaxes smooth muscle and decreases peripheral resistance. Alpha 1 Blocker used to inhibit Alpha1's vasoconstriction effects |
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Why would you choose to use a diuretic to treat chronic heart failure?
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Diuretics
Drug of choice for symptomatic relief of heart failure. Diuretics will reduce preload or the volume of blood that will fill the ventricle. Diuretic use is reserved for Class II - IV becuase these classes of heart failure are more likely to retain Na+ Thiazides are good for HTN because they are a weak diuretic. (but remember they are ineffective with decreased creatine clearance levels) Loop diuretics are used more often because of their increased strength and are also effective when CrCl <30 mL/min. Loops can be given as a first line drug if there is a significant amount of edema present. Also supplement with potassium which will decrease arrhythmias and decrease the risk of digoxin toxicity |
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Why would you choose to use a K+ sparing diuretic to treat chronic heart failure?
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Weak diuretics
However, if your patient needs a diuretic and could use a potassium supplement (to treat an underlying arrhythmia or decrease the risk of digoxin toxicity) an option would be to prescribe a K+ sparring diuretic. Always monitor K+ closely (especially with ACE inhibitors) because too much extracellular potassium (hyperkalemia) can cause an adverse effect and lead to "lethal" arrhythmias. Remember increased extracellular potassium will decrease the resting membrane potential and decrease the action potential, thus making contraction of the heart progressively weaker. "VFib/ Asystole" Spironolactone—drug of choice in K+ sparing class |
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When would an ACE inhibitor be contraindicated?
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Note: ARBs are an alternative when ACE inhibitors are not tolerated (except with angioedema)
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Why would you choose digoxin to treat chronic heart failure?
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Digoxin is not 1st choice, but it is a good medication to control the rate of the heart (slow it down) so, that the ventricles have enough time to fill properly.
Note: often when the heart is not working properly (Atrial Fibrillation/ Flutters) the heart can "quiver" and pump insufficiently. Digoxin decreases the conduction of electrical impulses through the AV node via inhibition of the Na+/K+ pump causing increased intracellular Na+ and Ca+ * Positive inotropic effect * Decreased sympathetic response * Decreased renin-angiotensin ouput This causes the inside of the cell to stay "positive/ depolarized" and when this occurs the voltage gated Na+ channels which were inactivated post initial depolarization stay inactivated. "Absolute Refractory Period" the time when no amount of stimulus can effect the membrane. Last, but not least digoxin increases vagal/ parasympathetic activity; decreased conduction at AV node. Can be used in addition to ACE inhibitor and diuretic therapy. |
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Why would you choose a Beta Blocker to treat chronic heart failure?
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You would choose a beta blocker when considering a stable patient already on ACE inhibitors and diuretics who are also experiencing tachycardia or arrhythmias.
Remember Beta 1 receptors bind to epi and norepi causing a sympathetic response (increased heart rate, increased contractility/ positive chronotropic and inotropic effects) Beta blockers thus block this response and will initially reduce cardiac output (negative chronotropic/ inotropic effects), but in return the sympathetic response is blocked and the heart rate will slow down and give the ventricles more time to fill properly. "work more efficiently" Beta Blockers are reserved for Class II and III (if no contraindications; for example 2nd or 3rd degree heart block, Asthma, COPD, Bradycardia, or Hypotension) |
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Why choose a Calcium Channel Blocker (DHPs) to treat chronic heart failure?
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You would choose to use a Caclium Channel Blocker (DHP) in addition to an ACE inhibitor/ diuretic therapy for a stable patient with uncontrolled hypertension or angina.
Remember calcium channel blockers block voltage-gated calcium channels in cardiac muscle and blood vessels. This decreases intracellular calcium leading to a reduction in muscle contraction allowing the arterial diameter to dilate. "vasodilation" decreasing peripheral resistance. The decreased contractility decreases cardiac output. The heart is pushing hard and the vessels aren't resisting. "Decreased Blood Pressure" * with low blood pressure, the afterload or amount of contraction needed to eject is decreased. This allows to work with less oxygen; decreased oxygen demand = decreased angina! Note: Calcium Channel Blockers do not affect the input of the sympathetic system and therefore allows the body to continue regulating the heart. When blood pressure is decreased the carotid baroreceptors will still sense this and send a sympathetic reflexive response to increase the heart rate. * Beta blockers can be given with Calcium channel blockers to minimize these effects |
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What class of drugs would you prescribe for a pt with a left ventricular systolic dysfunction?
Clue: This pt would not be able to take ACE inhibitors or ARBs |
Nitrates and Hydralazine
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Why would you choose an anticoagulant to treat chronic heart failure?
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You would choose an anticoagulant for patients with a low ejection fraction.
Warfarin |
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Patients with cardiac disease, w/o resulting limitations of physical activity. Ordinary physical activity does not cause undue fatigue, palpitations, dyspnea or angina
This describes which NYHA Heart Failure Classification? |
Class I
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Patients with cardiac disease, w/slight limitations of physical activity. Patients are comfortable at rest, but ordinary physical activity results in fatigue, palpitations, dyspnea or angina
This describes which NYHA Heart Failure Classification? |
Class II
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Patients with cardiac disease, w/limitations of physical activity. Patients are comfortable at rest, but less than ordinary physical activity results in fatigue, palpitation, dyspnea or angina
This describes which NYHA Heart Failure Classification? |
Class III
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Patients with cardiac disease, w/inability to carry on any physical activity without discomfort. Symptoms of cardiac insufficiency or of angina may be present at rest. If any physical activity is undertaken, discomfort is increased.
This describes which NYHA Heart Failure Classification? |
Class IV
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What type of medication would you prescribe if a patient could not take ACE inhibitors or Angiotensin Receptor Blockers (ARBs)?
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A Nitrate or Hydralazine (with caution)
Note: Nitrates provide rapid symptomatic relief in patients with acute exacerbation failure, but can produce or exacerbate hypotension, and it often causes a headache. Both topical and IV administration can be rapidly discontinued if necessary Hydralazine is a smooth muscle relaxant and can elicit a reflex sympathetic stimulation of the heart (the baroreceptor reflex.) The sympathetic stimulation may increase heart rate and cardiac output, and may cause angina or a MI. In addition hydralazine may increase plasma renin concentration resulting in fluid retention. *(used with a beta blocker and diuretic) to offset ADEs. These drugs both have considerable side effects and therefore 2nd line drugs. |
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Which NYHA Classes are diuretics reserved for and why?
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Class II through IV
These classes are more likely to retain Na+ |
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What is the drug of choice for symptomatic relief of heart failure?
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"Diuretics"
Thiazides are good for hypertension Chlorothiazide (Diuril) Hydrochlorothiazide Chlorthalidone (Hygroton) Indapamide (Lozol) Metolazone (Zaroxolyn) Loop diuretics however are often needed for extrastrength and its efficacy when CrCl < 30mL/min |
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Heart Failure can include many symptoms including very significant amounts of edema.
What type of diuretic would be your drug of choice in this situation? |
Loop Diuretic
Furosemide (Lasix) Torsemide (Demadex) Bumetanide (Bumex) |
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When prescribing loop diuretics what should you also prescribe to decrease the risk of arrhythmias and digoxin toxicity?
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Potassium supplement
Remember: This diuretic is very effective in blocking na+ reabsorption and because na+ is a huge osmotic component it has a greater risk of electrolyte imbalances (hypokalemia). Digoxin on the other hand has a narrow therapeutic index (the margin between effectiveness and toxicity). Adverse effects are more common in patients with hypokalemia, since it normally competes with K+ ions for the same binding site on the Na+/K+ ATPase pump. Remember that hypokalemia refers to low levels of potassium in the blood, however this means there is increased intracellular potassium/ potassium on the receptors. If digoxin cannot bind to the pump then it will accumulate in the blood and become toxic. |
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What is the K+ sparing diuretic drug of choice?
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Spironolactone
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What must you consider when prescribing Spironolactone with an ACE inhibitor?
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Hyperkalemia
Because ACE inhibitors and K+ sparing diuretics like Spironolactone can both lead to an increase in extracellular potassium. Remember: ACE inhibitors decrease aldosterone levels and aldosterone is responsible for increasing the excretion of potassium. |
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Which antagonist blocks the sympathetic response of the heart; Beta Blockers or Calcium Channel Blockers?
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Beta Blockers
provide a reduction in [norepinephrine] in the blood. |
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What class of heat failure are beta blockers reserved for?
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Class II and III
If no contraindications Remember beta blockers block the sympathetic response to the heart and therefore there is no "regulation" if blood pressure drops or if the heart rate is too low. Therefore contraindicated in NYHA Class IV 2nd and 3rd degree blocks Bradycardia Hypotension Note: non selective beta blockers are also not recommended in patients with asthma or copd. |
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Which Alpha- Beta Blocker is approved for Class II and III heart failure?
Clue: This drug is usually prescribed prior to discharge when the patient is stable and on an optimal dose of ACE inhibitor/ diuretic therapy. |
Carvedilol (Coreg)
(Available in Long Lasting Formula) |
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Which drug shares the same contraindications as a beta blocker and why?
NYHA Class IV heart failure 2nd and 3rd degree heart block Asthma/ COPD Bradycardia Hypotension |
Carvediol (Coreg)
It is an Alpha-Beta blocker Non Selective Beta Receptors and Alpha 1 Receptors specifically. This type of response inhibits vasoconstriction as well as bronchodilation. |
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Which Calcium Channel Blocker has been studied and appears to be safe for the treatment of heart failure?
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Amlodipine (Norvasc)
Used in conjunction with a ACE inhibitor/ diuretic treatment for patient's with uncontrolled hypertension and/or angina. |
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This drug is used for rate control for patients with heart failure whom are experiencing Atrial Fibrillation.
It is not metabolized via the Cyt P45 system and therefore has active metabolites with plenty of drug interactions!!!!!! |
Digoxin (Lanoxin)
Digoxin has many many drug interactions to consider, but remember they all have something in common. They all in some way alter metabolism or excretion and thus create an increase in serum levels/ toxicity! Verapamil (CCB,non)- reduces digoxin clearance ****Amiodarone (antiarrhythmic)- inhibition of digoxin secretion from renal tubules leading to toxic digoxin levels Thiazides- can cause potassium depletion and sensitize the myocardium to digoxin Quinidine- decrease renal clearance Azoles- decrease renal clearance Macrolides- affect the bacteria in the gut that is responsible for reducing absorption; therefore absorption is increased. |
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When is Digoxin absolutely contraindicated and why?
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Ventricular Fibrillation
Remember that digoxin inhibits the Na/K pump, which in return increases intracellular Na+ and Ca+ concentrations. Increased intracellular Ca+ can cause/ worse VFib |
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Digoxin Toxicity happens unknowingly very often and recognizing its symptoms is very important.
What might you see? |
Digoxin has a very small window of efficacy. It works well, but must be kept at an optimal level. ADE include:
Diarrhea, loss of appetite, nausea, vomiting, headaches, visual disturbances, weakness, confusion, cardiac dysrhythmias (PVCs and VTac), severe bradycardia, and even heart blocks Note: elderly patients with heart disease, renal dysfunction, hepatic dysfunction, hypothyroidism, and COPD are at an increased risk for toxicity. |
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How do you treat Digoxin Toxicity?
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Digibind or DigiFab
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Why are anticoagulants reserved for patients with low ejection fraction?
Give an example. |
Warfarin
When a patient has a low ejection fraction, the heart is not ejecting all of its blood. It will begin to pool in the vetricles and "clot". |
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What are the drugs of choice for diastolic dysfunction?
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*Low Doses to avoid hypotension
Diuretics (to reduce blood volume/ accumulation noted in the lungs) Nitrates (reduce LV volume by increase venous capacitance) Remember: Diastolic dysfunction refers to an abnormality in the heart's (i.e., left ventricle's) filling during diastole |
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Define acute heart failure.
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Medical emergency marked by sudden decrease in cardiac output due to either a natural disease progression or a precipitating factor
For example: Noncompliance w/tx, Uncontrolled HTN, Arrhythmias, Pulmonary infxn, stress, fluid overload, MI, Drugs—antiarrhythmics, non-DHP CCB’s, chemo, NSAID’s, glucocorticoids, hormones, high Na-containing drugs |
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What are your options when treating acute heart failure? (3)
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Diuretics (loops/Lasix)
Vasodilator (Nitroprusside/Nitroglycerin) Human Natriuretic Peptide Nesiritide (Natrecor) |
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How do diuretics help to treat acute heart failure?
Give an example. |
Decrease Preload
Loops/ Lasix |
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A patient in E.R. who has just suffered a MI is now experiencing Acute Heart Failure. What should you describe 1st?
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Loop Diuretic/ Lasix (1st choice)
decrease preload and effective for patients with a CrCl of <30 |
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When treatment (loop diuretic) for acute heart failure is refractory/ inadequate, what should you do?
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When heart failure is refractory/ inadequate and a loop diuretic is not enough, you should also prescribe a thiazide.
Loop + Thiazide = Synergestic Effect (monitor for hypokalcemia) |
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When treating acute heart failure what are your options?
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1st Loop Diuretic (Lasix)
2nd Loop + Thiazide - Vasodilators Sodium Nitroprusside (Nipride), Nitroglycerin -Human Natriuretic Peptide: Nesiritide (Natrecor) -Positive Inotropes Beta Agonists (Dopamine, Dobutamine) Phosphodiesterase inhibitors: PDE (Amrinone, Milrinone (Primacor)) |
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What are Nitroprusside and Nitroglycerin used to treat and how do they work?
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Acute Heart Failure Treatment
Vasodilators: decrease preload and afterload Sodium Nitroprusside (Nipride) will decrease PCWP and SVR Nitroglycerin will decrease PCWP * They can be added to IV loop diuretic administration to improve symptoms in patients without symptomatic hypotension. Pulmonary Capillary Wedge Pressure (PCWP)- indirect measurement of left atrial pressure Systemic Vascular Resistance (SVR)- resistance that must be overcome to move blood thru circulatory system |
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Nitroglycerin and Nitroprusside are used to treat acute heart failure. They are vasodilators. Which one will decrease PCWP and SVR?
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Sodium Nitroprusside (Nipride)
Used to tx malignant HTN (elevated bp with organ damage in the eyes, brain, lung and/or kidneys.) or for rapid control of bp during vascular surgery and neurosurgery. Pulmonary Capillary Wedge Pressure (PCWP)- indirect measurement of left atrial pressure Systemic Vascular Resistance (SVR)- resistance that must be overcome to move blood thru circulatory system |
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Give an example of a Human Natriuretic Peptide and what is it used to treat?
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Nesiritide (Natrecor)
Decreases PCWP & SVR Dec. norepi (sympathetic) & aldosterone Increases urinary output & Na excretion |
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Which drug used to treat heart failure could also cause cyanide/thiocyanate toxicity?
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Sodium Nitroprusside (Nipride) IV
It is bound to five molecules of cyanide (Na2[Fe(CN)5NO]) which are released when metabolized in the liver, but in order to be excreted it is added to thiosulfate = thiocynate. Note: T1/2 life is very short/ less than ten minutes, but its metabolites can linger for several days |
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What are the adverse effects of nitroglycerin?
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Hypotension (arterial and *venous vasodilation)
reflex tachycardia (bottom out and heart reflexively increases heart rate) **headache ("nitroglycerin head") tachyphylaxis (rapid decrease in the response to a drug after repeated doses over a short period of time, because the neurotransmitter in which it is affecting has become depleted and can no longer be stimulated.) |
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What is nitroglycerin used to treat and why does it work so quickly?
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Hypertensive crises and Acute coronary syndrome
In these cases the patient is experiencing signs and symptoms that indicate the heart is not getting enough oxygen (MI) T 1/2 Life is 1-4 mins |
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Combines w/sulfhydryl groups in vascular endothelium to create compounds which mimic nitric oxide’s stimulation of guanylate cyclase & production of cGMP (nitric oxide is a natural vasodilator)
This is the MOA for which drug? |
Nitroglycerin
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What is the Human Natriuretic Peptide used to treat Class IV acute heart failure?
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Nesiritides (Natrecor)
Nesiritide is indicated for the intravenous treatment of patients with acutely decompensated congestive heart failure who have dyspnea at rest or with minimal exertion. In these patients, the use of nesiritide is expected to reduce pulmonary capillary wedge pressure and improve dyspnea with fewer side effects than other intravenous agents (i.e. dobutamine, milrinone, nitroglycerine, nitroprusside). |
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Name the positive inotropes used to treat acute heart failure.
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*Beta Agonists (Dopamine, Dobutamine)
*Phosphodiesterase inhibitors: PDE (Amrinone, Milrinone (Primacor) Positive Inotropes relieve symptoms & improves end-organ fnxn in patients with decreased peripheral perfusion or end-organ dysfnxn if SBP <90 mmHg Patient would be symptomatic hypotension, but must have adequate filling pressure These drugs are used because the patient became refractory or intolerant of IV vasodilators. |
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This medication is used to treat acute heat failure it will:
Decrease PCWP (lt. atrial pressure) Decrease SVR (syst. resistance) Cause min chg to HR and CI Increase Urinary Ouput Increase Na+ Excretion Decrease norepi and aldosterone It is given IV and if the patient is hypotensive, bolus should be avoided. |
Nesiritide (Natrecor)
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What are the inotropic/ chronotropic effects of dobutamine (Dobutrex)?
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Positive
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What is dobutamine (Dobutrex) used for and when is it recommended?
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Acute Heart Failure
It is a positive inotrope/ Beta agonist (stimulate heart) Recommended when patient is also hypotensive. |
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*This drug stimulates dopamine and beta 2 receptors which increase perfusion to the brain and kidneys.
It also stimulates Alpha 1 and Beta 1 receptors to increase cardiac output |
Dopamine
Beta agonist (stimulate heart) |
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This drug stimulates beta 1 and beta 2 receptors which increase cardiac output and decrease systemic vascular resistance
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Dobutamine (Dobutrex)
Beta Agonist (stimulate heart) |
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What are the inotropic/ chronotropic effects of milrinone (Primacor)?
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+ inotropy
no chronotropic effects Recommended if receiving beta blocker (for rate control) |
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Normally these two drugs are given via IV; bolus first and then continuous infusion to treat acute heart failure.
However, when a patient is hypotensive its bolus dose should be avoided! |
Nesiritide (Natrecor): Human Natriuretic Peptide
Milrinone (Primacor) PDE Inhibitor/ Positive Inotrope (phosphodiesterase inhibitor) |
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These two positive inotropes are used to treat acute heart failure but, could actually increase mortality when used long term.
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Positive Inotropes:
Dobutamine (Dobutrex)/ Beta agonist Milrinone (Primacor)/ PDE inhibitor |
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What are phophodiesterase inhibitors used for and what do they do?
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Treat Acute Heart Failure
Positive Inotrope Increase Vasodilation and Increase Cardiac Output |
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Name two PDE inhibitors.
(phosphodiesterase inhibitors) |
Amrinone
Milrinone (Primacor) A phosphodiesterase inhibitor is a drug that blocks one or more of the five subtypes of the enzyme phosphodiesterase (PDE), therefore preventing the inactivation of the intracellular second messengers, cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP), by the respective PDE subtype(s). |
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What are the treatment options for stable angina?
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Antiplatelet agents
*Aspirin *Ticlopidine (Ticlid) *Clopidogrel (Plavix) BB’s CCB’s Nitrates |
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What are the treatment options for myocardial infarction (MI)?
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Glycoprotein IIb/IIIa Inhibitors
-Abciximab (ReoPro) -Eptifibatide (Integrilin) -Tirofiban(Aggrastat) |
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Heart Failure Classifications
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Class I- Pts with cardiac disease, w/o resulting limitations of physical activity. Ordinary physical activity does not cause undue fatigue, palpitations, dyspnea or angina
Class II- Patients with cardiac disease, w/slight limitations of physical activity. Patients are comfortable at rest, but ordinary physical activity results in fatigue, palpitations, dyspnea or angina Class III- Patients with cardiac disease, w/limitations of physical activity. Patients are comfortable at rest, but less than ordinary physical activity results in fatigue, palpitation, dyspnea or angina Class IV- Patients with cardiac disease, w/inability to carry on any physical activity without discomfort. Symptoms of cardiac insufficiency or of angina may be present at rest. If any physical activity is undertaken, discomfort is increased. |
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Types of Angina
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Stable
Angina on exertion Typical duration <20min Typically relieved with SL NTG Unstable Acute angina at rest Typically prolonged duration (>20min) ST-segment depression, T-wave inversion or no EKG changes NO biomarkers for cardiac necrosis present Non-ST-elevation Myocardial Infarction (NSTEMI) Non ST Elevation MI Same as UA + positive cardiac enzyme biomarkers of necrosis (troponin elevation), CKMB fraction >5-10% of total CK |
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Aspirin is used as an antiplatelet agent to treat stable angina.
It is metabolized in the liver (hepatic conjugation). Where is it hydrolyzed? |
Aspirin
Hydrolyzed in GI mucosa |
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What precautions should you consider when administering Clopidogrel (Plavix)?
Treatment for Stable Angina |
Thrombotic Thrombocytopenic Purpura TTP
rare disorder of the blood-coagulation system, causing extensive microscopic thromboses to form in small blood vessels throughout the body usually occurs within 1st 2 weeks |
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What precautions should you consider when administering Ticlopidine (Ticlid)?
Treatment for Stable Angina |
Thrombotic Thrombocytopenic Purpura TTP
Severe Hepatic Disease Aplastic anemia |
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A patient comes into the e.r. with stable angina, but is allergic to aspirin and clopidogrel (Plavix), what should you administer?
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Ticlopidine (Ticlid)
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Antiplatelet agents are used to treat stable angina, which one has the most adverse effects and what are they?
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Ticlopidine (Ticlid)
Bleeding , GI upset and Diarrhea Increased TC (8-10% w/in 1 mth of tx) & TG’s Neutropenia Hepatic dysfunction Thrombotic Thrombocytopenic Purpura TTP |
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How do beta blockers help treat stable angina?
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Reduces myocardial oxygen demand
Decreases HR, contractility Decreases BP Remember beta receptors are adrenergic receptors which respond to sympathetic stimulation. |
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What type of beta blocker should you choose to treat a patient with stable angina?
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Cardioselective Beta Blockers
For example: Beta 1 Blockers Metoprolol (Lopressor, Toprol XL), atenolol (Tenormin), acebutolol (Sectral), esmolol (Brevibloc) |
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A patient comes in with signs of ischemia:
Angina SOB Nausea/Vomiting Diaphoresis “silent ischemia” potentially caused by diabetic neuropathy, chemical release altering pain perception When do you decide to give a beta blocker? |
Beta blockers are 1st agents for Ischemic Heart Disease.
If a patient has one or more of the following: Angina resulting from physical exertion Concurrent HTN Concurrent supraventricular arrhythmias Post-MI angina Angina induced by anxiety |
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Beta blockers are initiated as a monotherapy to treat ischemic heart disease, but if they are ineffective what can you do?
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Choice One- Add a nitrate
(SL Nitroglycerin or patch, Isosorbide dinitrate, Isordil, Imdur, Ismo) * Decreases myocardial oxygen demands by venodilation & arterial dilation Choice Two- Replace with Calcium Channel Blocker Non DHPs preferably (Diltiazem ,Verapamil) *Remember non DHPs work directly on the myocardium to decrease heart rate and cardiac ouput (exception would be if the patient has heart failure due to left ventricular systolic dysfunction, in which CCB are contraindicated) |
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If a patient does not improve with a beta blocker nor with the addition of a nitrate (option one), and a calcium channel blocker must be considered, what are the contraindications for DHPs and Non DHPs?
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Remember Non DHPs are the first choice (Diltiazem ,Verapamil), but they are contraindicated in heat failure with left ventricular systolic dysfunction. With heart failure the heart is already not pumping efficiently and with a ccb that directly affects the myocardium you will inhibit the ability that is functioning.
**************Coronary artery vasospasm—choose diltiazem************* _________________________________________ DHPs are contraindicated post MI because of the reflex tachycardia reaction. This occurs when blood pressure decreases and the heart counteracts and increases its rate to compensate. Amlodipine (Norvasc), Nifedipine (Adalat, Procardia) ending in -dipine *************Ventricular dysfunction—choose amlodipine******** |
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How do Non DHPs (1st choice) differ from DHPs when treating Ischemic Heart Disease?
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*Non-DHP’s work directly on the myocardium(Diltiazem ,Verapamil)
Depresses AV node conduction (dec. heart rate) Negative inotrope (decrease contractility)/ Vasodilation, afterload reduction (decrease cardiac output) __________________________________ *DHPs (last choice) work directly on the vasculature decrease peripheral vascular resistance Amlodipine (Norvasc), Nifedipine XL (Adalat, Procardia)/ Long Acting Formula |
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How do nitrates work?
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Decreases myocardial oxygen demands by venodilation & arterial dilation
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Isosorbide dinitrate/mononitrate (Isordil, Imdur, Ismo)
What type of drugs are these and what are they used for? |
Nitrates to treat ischemic heart disease by decreasing myocardial oxygen deamands by venodilation and arterial dilation.
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Can sublingual nitroglycerin be used as a preventative measure when you know that shoveling the snow today will more than likely give you angina?
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NO
But, Isosorbide is a preventative nitrate medication |
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How would you administer sublingual nitroglycerin and how often can you give it?
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Dosing: 1 tablet (0.4mg) SL x 1 for chest pain
May repeat w/1 tablet every 5 min for max of 3 tablets If no relief after 3 tablets, EMS |
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What is nitrate tolerance?
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*Nitrates must be converted inside vascular smooth muscle cells into nitric oxide.
This conversion can only occur when a nitrate is added to cysteine resulting in nitric oxide. It is the nitric oxide that leads to vasodilation! If you give your cells are exposed to nitrates over and over they can become depleted of cysteine and can no longer convert the nitrate into nitric oxide. (rapid onset w/in 24hrs) To prevent this or reverse it once it has occurred allow 8-12 hrs before administering any more nitrates. |
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What are the contraindications for Isosorbide?
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Concurrent with any erectile dysfunction medications:
Sildenafil (Viagra),Vardenafil (Levitra) or Tadalafil (Cialis) Closed angle glaucoma (here the drainage canals are already blocked and Isosorbide would vasodilate increase blood flow. ) head trauma or cerebral hemorrhage (can increase intracranial pressure) |
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When would you administer Nitroglycercin IV, when would you administer it sublingual or via patch?
Remember nitroglycerin is a vasodilator! |
Nitroglycerin IV is used to treat acute heart failure
Nitroglycerin Sublingual/Patch is used to treat ischemic heart disease |
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Abciximab (ReoPro)
Eptifibatide (Integrilin) Tirofiban(Aggrastat) What are these meds and what are they used for? |
Glycoprotein IIB/ IIIA Inhibitors
used to treat ischemic heart disease/ acute coronary syndrome with percutaneous innervation (PCI) Blocks glycoprotein IIb/IIIa receptor site which is binding site for fibrinogen and Factor VIII; reversibly blocks platelet aggregation Indication: Acute coronary syndrome w/PCI |
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What type of drug is indicated for treatment of acute coronary syndrome with percutaneous innervation?
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Glycoprotein IIB/ IIIA Inhibitors
Note: studies have shown that there is also a good outcome when used in addition to Bivalirudin (Angiomax) a direct thrombin inhibitor |
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Why would you choose Abciximab (ReoPro) versus Eptifibatide (Integrilin) or Tirofiban(Aggrastat)?
Glycoprotein IIB/ IIIA Inhibitors |
ReoPro is large MW drug,Strongest bond to GP IIb/IIIa receptor; Effects last 48hrs; Need platelet transfusion to reverse
FYI: during a percutaneous intervention procedure clots can form and cause the patient to have a heat attack. Reo Pro reduces the chance of clot formation and is often combined with aspirin or heparin during the procedure. Others are low MW & weaker binding to receptor; Reverse effects by stopping infusion; Effects wear off in 4hrs |
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What are the adverse of effects worth considering when administering a Glycoprotein IIB/ IIIA Inhibitors?
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Bleeding, Hypotension, Thrombocytopenia
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Give an example of a direct thrombin inhibitor and when its use would be indicated.
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Bivalirudin (Angiomax)
Indicated in unstable angina (UA) undergoing PCI Note: Studies have shown good outcomes when used in place of heparin as monotherapy and also in conjunction with GP IIb/IIIa inhibitors |
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What are some adverse effects that should be considered when using Bivalirudin (Angiomax)
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Bleeding, hypotension (less than heparin), h/a, CNS pain, nausea, bradycardia
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