Heart Failure - Treatment Flashcards
<p>What is heart Failure Characterised by?</p>
<p>–by progressive cardiac dysfunction</p>
<p>–breathlessness</p>
<p>–tiredness</p>
<p>–neurohormonal disturbances</p>
<p>–sudden death</p>
<p>What is congestive heart failure defined as?</p>
<div>Heart unable to pump blood that meets the demands of the tissues or it can do so but only from high pressures.</div>
<p>What are the two types of heart failure?</p>
<p><strong>Systolic heart failure</strong> - Decreased pumping function of the heart, which results in fluid back up in the lungs and heart failure</p>
<p>Diatolic heart failure</p>
<p>(HFrEF - heart failure with presereved ejection fraction)</p>
<p></p>
<p>Diastolic Heart Failure - Thickened and stiff heart muscle</p>
<p>- Heart does not fill properly with blood</p>
<p>- Fluid back up in the lungs and hear failure</p>
<p>(HFpEF) - Heart failure with preserved ejection fraction</p>
<p>Risk factors for heart failure</p>
<p>•Coronary artery disease</p>
<p>•Hypertension (LVH)</p>
<p>•Valvular heart disease</p>
<p>•Alcoholism</p>
<p>•Infection (viral)</p>
<p>•Diabetes</p>
<p>•Congenital heart defects</p>
<p>•Other:</p>
<p>–Obesity</p>
<p>–Age</p>
<p>–Smoking</p>
<p>–High or low hematocrit level</p>
<p>–Obstructive Sleep Apnea</p>
<p>What is the effect of heart failure on Frank - Starling Law?</p>
<p>Failing heart causes the relationship to be lost - amount of stretch is no longer proportional to the force of contraction</p>
<p>Circulatory volume increases - heart dilates - force of contraction reduces and there is a further drop in cardiac output.</p>
<p>Activation of the RAAS (renin angiotensin aldosterone system)</p>
<p>When does heart failure usually occur?</p>
<p>Following sustained hypertension</p>
<p>As a result of myocyte damage - MI</p>
What is the result of a reduced cardiac output on blood pressure?
<p>What is the effect of–Atrial and Brain Natriuretic Peptides?</p>
<p>•Potent vasodilators and natriuretic peptides</p>
<p>•Short halflife</p>
<p>What are the drugs for the treatment of symptoms?</p>
<p>•Diuretics</p>
<p>•Digoxin</p>
<p>What is the treatment for the improvement of symptoms and survival?</p>
<p>•ACE inhibitors/ARBs</p>
<p>•Spironolactone</p>
<p>•Valsartan-sacubitril</p>
<p>What are the goals of treatment?</p>
<p>•Symptomatic treatment</p>
<p>•Inhibition of detrimental neurohormonal adaptations</p>
<p>•Enhancement of beneficial neurohormonal adaptations</p>
<p>•Enhancement of cardiac function</p>
<p>Give examples of loop diuretics</p>
<p>–FUROSEMIDE or BUMETANIDE</p>
<p>How is sympathetic activation blocked?</p>
<p>Beta blockers - in this case:</p>
<p></p>
<p>–CARVEDILOL, BISOPROLOL and METOPROLOL are beta blockers which are of proven benefit in the treatment of CHF</p>
<p>What are the two types of drugs that block the effects of angiotensin 2?</p>
<p>Ace inhibitors (Rampril)</p>
<p>Angiotensin antagonists</p>
<p>How is aldosterone blocked?</p>
<p>Spironolactone -Produces a significant reduction in morbidity</p>
<p>What are the beneficial hormonal changes that we want to enhance?</p>
<p>Natriuretic peptide system</p>
<p>What metabolises brain and heart natriuretic peptides?</p>
<p>Neutral endopeptidse</p>
<p>What is the effect of digoxin?</p>
<p>Enhances cardiac function - improves cardiac statue</p>
<p>Digoxin toxicity is a very likely</p>
<p>What is the effect of vasodilators?</p>
<p>Reduce preload and afterload - improving cardiac function</p>
<p>–Hydralazine an arterial dilator has also been shown to improve cardiac function</p>
<p>Give examples of vasodilators</p>
<p>ISOSORBIDE MONO or DINITRATE</p>
<p>How do loop diuretics work?</p>
<p>Inhibit the sodium potassum chlorine transporter in the loop of henle- inducing profound diuresis.</p>
<p>What are the adverse drug reactions for diuretics?</p>
<p>–Dehydration</p>
<p>–Hypotension</p>
<p>–Hypokalaemia, Hyponatraemia</p>
<p>–Gout</p>
<p>–Impaired glucose tolerance, diabetes</p>
What are the drug drug interactions with frusemide?
<p>What are the drugs needed for reducing mortality?</p>
<p>•Angiotensin Blockade</p>
<p>•Beta receptor blockade</p>
<p>•Aldosterone blockade</p>
<p>•ANP/BNP enhancement</p>
<p>What are the relevant ACEi?</p>
<p>RAMIPRIL, ENALAPRIL, LISINOPRIL</p>
<p>What are the adverse drug reactions of ACEi?</p>
<p>–First dose hypotension</p>
<p>–Cough</p>
<p>–Angioedema</p>
<p>–Renal impairment</p>
<p>–Renal failure</p>
<p>–Hyperkalaemia</p>
<p>What are the drug drug interactions with ACEi?</p>
<div>–NSAIDs acute renal failure</div>
<div>–Potassium supplements hyperkalaemia</div>
<div>–Potassium sparing diuretics hyperkalaemia</div>
<p>How does the effectiveness of ARB's compare with ACEi?</p>
<p>NOT as effective</p>
What is the role of AT1 and AT2 receptors?
ARB’s act on the AT1 receptor
<p>What is the role of AT1 and AT2 receptors?</p>
<p>ARB's act on the AT1 receptor</p>
<p>What is the effect of neprilysin?</p>
<p>Stops break down of BNP and ANP by neutral endopeptidases</p>
<p>What is Valsartan - Sacubitril?</p>
<p>Combined valsartan and ARB and Neprilysin</p>
<p>What is the effect of spironolactone?</p>
<p>Aldosterone antagonist</p>
<p>Potassium sparing diuretic</p>
<p>Acts in distal tubule</p>
<p>Used in combination with loop diuretics</p>
<p>Particularly useful in resistant oedema</p>
<p>Proven to reduce mortality when used in combination with ACEI's</p>
<p>What is the major risk attached to beta blockers?</p>
<p>May precipitate severe deterioration in CHF</p>
<p>When type of onset are beta blockers used for?</p>
<p>–Should be used only when a patient has been stabilized and not during an acute presentation</p>
<p>What is the aim of ivabradine?</p>
<p>To improve survival</p>
<p>What is the effect of Ivabridine?</p>
<p>Specific inhibitor of current in sinoatrial node</p>
<p>•No action on other channels in the heart or vascular system.</p>
<p>•Does not modify myocardial contractility and intracardiac conduction, even in patients with impaired systolic function.</p>
<p>Whos is Ivabridine recommended for?</p>
<p>Stable chronic HFrEF</p>
<p>Maximum tolerated dose of beta blockers</p>
<p>In sinus rhythm</p>
<p>Have a heart rate of 70 bpm or greater at rest</p>
<p>What are the effects of Digoxin?</p>
<p>Increases the availability of calcium in the myocyte</p>
<p>No effect on mortality but it can reduce hospitilisations</p>
<p>Narrow therapeutic index</p>
<p>What are the side effects of digoxin?</p>
<p>Arrhythmias</p>
<p>Heart block</p>
<p>Nausea</p>
<p>Confusion</p>
<p>What is the purpose of warfarin in the treatment of heart failure?</p>
<p>–Dilated ventricle gives rise to thrombus formation and thrombo-embolic events</p>
<p>–Warfarin has proven value in preventing these events</p>
<p>What is the therapeutic regime?</p>
<p>Where ARNI is the Valsartan and Salcubitril (Neprilysin)</p>
<p>How do you monitor benefit?</p>
<p>Measuring weight is the only effective way to measure the loss on body fluids - urine volumes are unreliable</p>
