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Inotropics
UVa med pharmacology block 3
| Question | Answer |
|---|---|
| At what stage of HF are b-blockers CONTRAindicated? | Stage IV ***they are also not used in stage I, but mostly because not necessary |
| Describe the mechanism of action the Cardiac Glycosides (digoxin, digitoxin) in the heart? | - Inhibit basolateral Na/K pump - Reduces transmembrane gradient of Na -> reduces the activity of the Na/Ca exchanger-> less Ca is extruded - This causes increased Ca in the sarcoplasmic reticulum, thus greater contractility with every action potential |
| In addition to increases in the RAA system, what two other hormones are increased during HF? | - ANP - ADH |
| What is the goal of vasodilator therapy in CHF? How are they goals achieved (mechanism) | Reduce both preload and afterload Preload --> increase venous capacitance Afterload --> decrease TPR |
| Which generations of beta blockers are 1) not used, 2) used, 3) most efffective in treating HF? Give examples of each | 1) not used --- 1st generation (propanolol) 2) used --- 2nd generation (metoprolol) 3) most effective -- 3rd generation (carvedilol) |
| What is the difference between right and left sided heart failure? | Right: blood accumulates in systemic veins leading to dialation of liver and spleen, edema, ascites, etc. Left: blood accumulates in the pulmonary circulation leading to pulmonary congestion, cyanosis, dyspnea |
| What is low output heart failure? What is the difference between systolic and diastolic failure? | - Inability of myocardium to supply adequat blood volume to the body - SYSTOLIC: inability to contract sufficiently during systole - DIASTOLIC: inability to dialate sufficiently during diastole |
| What is the therapeutic status of Aldosterone receptor blockers in HF? What is the new drug that is promising and why? | - VERY effective when administered on top of standard therapy (ACEI + diuretic +/- dig) - Eplerenone --> free of sexual side-effects and effective in CHF |
| Why is sympathetic activation during Stage I failure beneficial? | - increased contractility - increased preload - increased RAA system ***compensates for the mild decrease in basal inotropic state |
| What are the immediate and chronic effects of cardiac glycosides? | IMMEDIATE --> increased contractility and ventricular function OVER TIME - increased CO -> improved renal perfusion -> excretion of fluid by kidneys - Increases cardiac fx & vagal tone, decr symp tone -> improved myocardial perfusion and O2 consumpt |
| What kind of drug is dobutamine? How is it used in HF and why? | - B1/B2 agonist - used ACUTELY, when digitalis, diuretics, and vasodialators have failed - increases contractility and not HR - increases short term circulation in decompensated patients |
| What are the main indications for digoxin? | - Heart failure with SYSTOLIC dysfunction - NOT reccomended for diastolic dysfunction - Supraventricular Tachyarrythmias - A FIB, a fluttler, atrial and nodal tachycardia |
| What are the is most effective type of diuretic used in CHF? Why? When are they started? | - Loop diuretics - they are more effective at promoting Na and water loss the other diuretics - can exert their effects despite low GFR - started at Stage II HF |
| What are the main causes of predominantly diastolic heart failure? | - chornic hypertension and hypertrophic cardiomyopathy |
| What precautions should you take with patients on digoxin? How do you treat overdose? | - Monitor drugs levels, ion levels - Overdose 1. withdraw drug 2. if mild, correct imbalance 3. if severe, give digitalis antibodies (DIGBIND) |
| What is the difference between digoxin and digitoxin? | - Digitoxin is more lipid soluble - Digitoxin is excreted by the liver, Digoxin by the kidneys - Digitoxin is NOT used very much (but need to know for Boards) |
| What is the most important side-effect of digoxin? Why is it an issue? | - Serious dysrythmias can occur - Dig. has a low therapeutic window, and many interactions with ions and drugs |
| When are Angiotensin Receptor blockers/isosorbide dinitrate/hydralizine used in CHF? What are their therapeutic differences to ACEI's? | - sub in cases of ACEI intolerance - AT1 -> less efficacious because no bradyknin (vasodialator) production *beneficial in ADDITION to ACEI's, not ALL Ang II production is blocked with ACEI -isosorbide lowers preload, hydralazine lowers afterload |
| T or F: Digoxin prolongs life when used in combination with diuretics and other heart failure medicines | FALSE Digoxing improves QUALITY of life, but has not been shown to prolong it |
| What are some important differences in the treatment of systolic vs. diastolic HF? | - Not as clear evidence in diastolic treatment - digoxin in controversial in diastolic treatment - Ca-blockers are effective in diastolic treatment |
| How is dopamine used in HF and why? How does it compare with dobutamine? | - D1 receptors vasodialates renal artery and coronaries --> decrease work of heart - At higher doses is a B1 agonist, so increases contractility (good) but also HR (bad) - LESS effective than dobutamine |
| What is the name of the trial that showed the benefits of using spironolactone in addition fo diuretics, ACEI, and dig? Whay are there benefits? | - RALES trial - Benefit from diuretic effect -> potentiates diuresis, spares K and Mg (anti-arrythmic) - Benefits from Aldosterone blockade -> Aldo increases CNS symp flow, myocardial remodeling/fibrosis, and potentiates effects of NE on heart |
| What three factors make digoxin the most commonly used drug? | - favorable pharmacokinetics - flexibility or administration route - excellent biochemical assays |
| Why is sympathetic activity increased in heart failure? | - Decreased inhibitory baroreceptor activity - Increased peripheral sympathetic activators (from heart and ischemic tissues) - Increased Ang. II and aldosterone activate sympathetic system |
| How is Digoxin excreted? What condition interferes with excretion? What type of drugs interfere with excretion? | - Excreted in urine - Renal disease interferes - CV drugs interfere |
| What ion conditions affects digoxin efficacy and how? | K+ hyper - decreases efficacy since Dig. binds to K+ site on Na/K pump hypo - increases efficacy Ca+ hyper - digoxin induced arrythmias since Dig. increases Ca+ stores Mg+ hypo - increases Dig. induced arrythmias, Mg seems to have opposite effect of |
| What are primary and secondary causes of heart failure? | Primary: coronary artery disease, cardiomyopathy, valvular disease, pericardial disease, myocarditis, congenital defects Secondary: systemic hypertension, anemia, thyrotoxicosis, PE, toxicity, etc. |
| When is Sodium Nitroprusside used in HF and why? Why must BP be adequate for usage? | - used ACUTELY for decompensated patient - dialates both arteries and veins - BP must be adequate to insure renal and cerebral perfusion |
| When are phosphodiesterase inhibitors used in HF? What is their effect on heart and vasculature? give mechanism | - used ACUTELY, can increased mortality chronically - in heart are inotropes --> increase cAMP --> increase Ca release --> contractility - in vasculature --> relaxation by increaseing cAMP and cGMP levels |
| Why are Thiazides not useful in Stage II HF and above? | Their already small natiruretic effect is further diminshed by a reduction in GFR (unlike loop diuretics) |
| How do plasm levels of NE correlate with stage of disease? | Higher NE levels indicate higher severity and worse prognosis |
| When are calcium channel blockers used in CHF? WHY-EEE? What class of blockers is used? | - Used in DIASTOLIC dysfunction **can make things worse in systolic dysfunction - facilitate filling and diastolic relaxation - verapamil and diltiazem (not DHP's) |
| Other than the heart, what two other places is Digoxin effective? Desribe the effect? | Diaphragm --> increased strength of breathing Peripheral nerves --> potentiates baroreceptor reflex, increases depolarization and thus makes them more sensitive |
| What stages of HF benefit from beta blocker usage? What is the therapeutic regimen? | - II and III - in COMBINATION with diuretics and ACEI's *** 3rd line therapy |
| What are the three important aspects of ACEI's in CHF therapy? | - FIRST LINE DRUG, started as soon as HF is diagnosed - shown to reduce mortality - main side effects are usually mild |
| - What are contraindications of b-blocker usage in HF? What MUST be corrected in a patient with CHF before starting b-blocker therapy and why? | - Reduced contractiliy, bradycardia, heart block, sick sinus rythmn - MUST correct fluid overload ***since a decrease in contractility would only make things worse |
| Why is sympathetic activation during later stages of heart failure detrimental? | - myocardial remodeling (AT receptors) - more O2 demand than supply - Arrythmias - cardiac toxicity |
| What neuroendocrine changes occur in response to low output failure? Are these changes beneficial or detrimental? | - Massive renal Na and H2O retention via increased symp output, renin, & aldosterone - Increased symp output *increased CO by increased contractility and rate *increased BP due to arteriolar constriction - At FIRST beneficial, later become detriment |
| What is the rationale for using b-blockers in HF (4 parts) | - lower renin (B1 blockade) - increase diastolic relaxation and reduce O2 consumption - reduced direct cardiotoxicity of NE - protection against arrythmias and Vfib |
Created by:
sam.mrosenfeld
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