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02. Cardiovascular System > Heart Failure - Treatment > Flashcards

Heart Failure - Treatment Flashcards

1
Q

<p>What is heart Failure Characterised by?</p>

A

<p>–by progressive cardiac dysfunction</p>

<p>–breathlessness</p>

<p>–tiredness</p>

<p>–neurohormonal disturbances</p>

<p>–sudden death</p>

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2
Q

<p>What is congestive heart failure defined as?</p>

A

<div>Heart unable to pump blood that meets the demands of the tissues or it can do so but only from high pressures.</div>

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3
Q

<p>What are the two types of heart failure?</p>

A

<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>

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4
Q

<p>Risk factors for heart failure</p>

A

<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>

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5
Q

<p>What is the effect of heart failure on Frank - Starling Law?</p>

A

<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>

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6
Q

<p>When does heart failure usually occur?</p>

A

<p>Following sustained hypertension</p>

<p>As a result of myocyte damage - MI</p>

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7
Q

What is the result of a reduced cardiac output on blood pressure?

A
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8
Q

<p>What is the effect of–Atrial and Brain Natriuretic Peptides?</p>

A

<p>•Potent vasodilators and natriuretic peptides</p>

<p>•Short halflife</p>

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9
Q

<p>What are the drugs for the treatment of symptoms?</p>

A

<p>•Diuretics</p>

<p>•Digoxin</p>

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10
Q

<p>What is the treatment for the improvement of symptoms and survival?</p>

A

<p>•ACE inhibitors/ARBs</p>

<p>•Spironolactone</p>

<p>•Valsartan-sacubitril</p>

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11
Q

<p>What are the goals of treatment?</p>

A

<p>•Symptomatic treatment</p>

<p>•Inhibition of detrimental neurohormonal adaptations</p>

<p>•Enhancement of beneficial neurohormonal adaptations</p>

<p>•Enhancement of cardiac function</p>

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12
Q

<p>Give examples of loop diuretics</p>

A

<p>–FUROSEMIDE or BUMETANIDE</p>

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13
Q

<p>How is sympathetic activation blocked?</p>

A

<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>

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14
Q

<p>What are the two types of drugs that block the effects of angiotensin 2?</p>

A

<p>Ace inhibitors (Rampril)</p>

<p>Angiotensin antagonists</p>

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15
Q

<p>How is aldosterone blocked?</p>

A

<p>Spironolactone -Produces a significant reduction in morbidity</p>

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16
Q

<p>What are the beneficial hormonal changes that we want to enhance?</p>

A

<p>Natriuretic peptide system</p>

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17
Q

<p>What metabolises brain and heart natriuretic peptides?</p>

A

<p>Neutral endopeptidse</p>

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18
Q

<p>What is the effect of digoxin?</p>

A

<p>Enhances cardiac function - improves cardiac statue</p>

<p>Digoxin toxicity is a very likely</p>

19
Q

<p>What is the effect of vasodilators?</p>

A

<p>Reduce preload and afterload - improving cardiac function</p>

<p>–Hydralazine an arterial dilator has also been shown to improve cardiac function</p>

20
Q

<p>Give examples of vasodilators</p>

A

<p>ISOSORBIDE MONO or DINITRATE</p>

21
Q

<p>How do loop diuretics work?</p>

A

<p>Inhibit the sodium potassum chlorine transporter in the loop of henle- inducing profound diuresis.</p>

22
Q

<p>What are the adverse drug reactions for diuretics?</p>

A

<p>–Dehydration</p>

<p>–Hypotension</p>

<p>–Hypokalaemia, Hyponatraemia</p>

<p>–Gout</p>

<p>–Impaired glucose tolerance, diabetes</p>

23
Q

What are the drug drug interactions with frusemide?

A
24
Q

<p>What are the drugs needed for reducing mortality?</p>

A

<p>•Angiotensin Blockade</p>

<p>•Beta receptor blockade</p>

<p>•Aldosterone blockade</p>

<p>•ANP/BNP enhancement</p>

25
Q

<p>What are the relevant ACEi?</p>

A

<p>RAMIPRIL, ENALAPRIL, LISINOPRIL</p>

26
Q

<p>What are the adverse drug reactions of ACEi?</p>

A

<p>–First dose hypotension</p>

<p>–Cough</p>

<p>–Angioedema</p>

<p>–Renal impairment</p>

<p>–Renal failure</p>

<p>–Hyperkalaemia</p>

27
Q

<p>What are the drug drug interactions with ACEi?</p>

A

<div>–NSAIDs acute renal failure</div>

<div>–Potassium supplements hyperkalaemia</div>

<div>–Potassium sparing diuretics hyperkalaemia</div>

28
Q

<p>How does the effectiveness of ARB's compare with ACEi?</p>

A

<p>NOT as effective</p>

29
Q

What is the role of AT1 and AT2 receptors?

A

ARB’s act on the AT1 receptor

30
Q

<p>What is the role of AT1 and AT2 receptors?</p>

A

<p>ARB's act on the AT1 receptor</p>

31
Q

<p>What is the effect of neprilysin?</p>

A

<p>Stops break down of BNP and ANP by neutral endopeptidases</p>

32
Q

<p>What is Valsartan - Sacubitril?</p>

A

<p>Combined valsartan and ARB and Neprilysin</p>

33
Q

<p>What is the effect of spironolactone?</p>

A

<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>

34
Q

<p>What is the major risk attached to beta blockers?</p>

A

<p>May precipitate severe deterioration in CHF</p>

35
Q

<p>When type of onset are beta blockers used for?</p>

A

<p>–Should be used only when a patient has been stabilized and not during an acute presentation</p>

36
Q

<p>What is the aim of ivabradine?</p>

A

<p>To improve survival</p>

37
Q

<p>What is the effect of Ivabridine?</p>

A

<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>

38
Q

<p>Whos is Ivabridine recommended for?</p>

A

<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>

39
Q

<p>What are the effects of Digoxin?</p>

A

<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>

40
Q

<p>What are the side effects of digoxin?</p>

A

<p>Arrhythmias</p>

<p>Heart block</p>

<p>Nausea</p>

<p>Confusion</p>

41
Q

<p>What is the purpose of warfarin in the treatment of heart failure?</p>

A

<p>–Dilated ventricle gives rise to thrombus formation and thrombo-embolic events</p>

<p>–Warfarin has proven value in preventing these events</p>

42
Q

<p>What is the therapeutic regime?</p>

A

<p>Where ARNI is the Valsartan and Salcubitril (Neprilysin)</p>

43
Q

<p>How do you monitor benefit?</p>

A

<p>Measuring weight is the only effective way to measure the loss on body fluids - urine volumes are unreliable</p>

02. Cardiovascular System (72 decks)

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