Pharmacology - CV Drugs 3 - Flashcards in University Pharmacy

What is chronic heart failure?

When CO falls to the point where it is insufficient to provide enough blood for the body's metabolic needs or when CO can only be maintained at sufficient levels by an elevated end-diastolic pressure (compensated)

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What are the mains of drug treatment? (1)

Reduce symptoms and improve quality of life (reduce oedema - pulmonary/systemic, increase exercise intolerance, increase myocardial contractibility, in acute HF) - diuretics, digoxin, lifestyle changes

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What are the mains of drug treatment? (2)

To slow progression and lengthen survival (decrease stimuli leading to hypertrophy and remodelling. Slow progressive worsening of symptoms and lengthens survival in CHF) - neurohormonal modulators, ACE-I, ARB, B blockers, aldosterone antagonists

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What are the mains of drug treatment? (3)

ARNI, ivabradine. Must also treat underlying and precipitating factors/co-morbidities (e.g. AF, hypertension, ischaemia, angina)

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Outline the history of CHF (1)

1940-70 - cardiorenal model - reduce CO. Forward failure (reduced CO to kidneys - fluid retention, oedema, fatigue). Backward failure (reduced CO, increased central/pulmonary venous pressure/oedema) - use diuretics

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Outline the history of CHF (2)

1970-1990 - cardiocirculatory model - reduced CO and vascular constriction led to fluid retention, oedema, fatigue, increases afterload, use PDE inhibitors, b1 receptor activation, increase cAMP in myocytes

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Outline the development of the neurohormonal model of CHF progression (1)

Proposals of activation of RAA and sympathetic NS. Clinical trials - vasodilators decrease BP/increase EF had no effect/increased mortality and symptoms. ACE-I enalopril reduced mortality. PDE-I milrinone improved EF but worsened symptoms/mortality

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Outline the development of the neurohormonal model of CHF progression (2)

Beta blockers reduced cardiovascular mortality in CHF due to ischaemic heart disease. Endogenous neurohormonal systems activated by initial injury to heart extent - direct toxic effect on myocardium. B blocker metoprolol reduced CV mortality in CHF

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Describe the effects of reduced CO in a healthy patient

Blood loss, reduced CO, decrease renal perfusion, activate RAA, restore blood volume, restore LVEDP (Starling), decrease in BP/volume increases sympathetic drive. Both restores CO/BP (short term process)

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Describe the effects of reduced CO in a CHF patient

Reduced CO, reduced renal perfusion/BP. RAA/sympathetic drive activated, increase blood volume, increase LVEDP but there is cardiac remodelling, reduced CO further, pulmonary oedema, arrhythmias (long term)

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What are the two types of CHF?

Reduced ejection fraction (systolic, <40%) and preserved ejection fraction (diastolic, >40%). Patients have combination - treated as CHF with reduced ejection fraction

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What are the NICE guidelines for treatment of CHF with reduced ejection fraction? (1)

ACE-I + B-blocker + diuretic (use ARB if ACE-I not tolerated). Add mineralcorticoid receptor antagonist (consider ivabradine if LVEF <35% and HR > 75 bpm), add sacubatril/valsartan if on ACE-I/ARB and LVEF <35%, digoxin for severe CHF

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What are the NICE guidelines for treatment of CHF with reduced ejection fraction? (2)

Consider hydralazine and nitrate if Afro-Caribbean and moderate-severe CHF

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Describe features of ACE-inhibitors (1)

E.g. ramipril. Slow progression of cardiac remodelling (hypertrophy and fibrosis). Vasodilate - reduced preload/afterload - reduce cardiac work - increase CO. Diuretic effect. Decrease symptoms (exercise intolerance, oedema)

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Describe features of ACE-inhibitors (2)

Slow progression of disease, lengthen survival - first line dug given for most HF patients. ADRs - chronic cough (use ARB instead), hypotension, renal failure, hyperkalaemia

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Describe features of ARBs

E.g. losartan. Block effect of Ang II exerted via stimulation of AT-1 receptors. Same beneficial effects on survival/symptoms as ACE-I without causing cough. Side effects/CIs similar. ARB combined with ACE-I when symptoms persist (reduce mortality)

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Describe features of beta-adrenoreceptor blockers (1)

Carvedilol (a1/non-selective b-blocker), bisprolol (b1 cardioselective). Prolong survival. Reduce HF symptoms/sudden death/cardiac remodelling/renin release. Negative iontropic (low doses, increased over months). CI in asthmatics

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Describe features of beta-adrenoreceptor blockers (2)

ACE-I + ARB + B-blockers combination is not recommended

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Describe features of aldosterone antagonists

Spironolactone. Reduce mortality in severe HF when added to standard therapy due to reduced fibrosis/remodelling of heart. But can cause gynaecomastia, hyperkalaemia, renal dysfunction (less gynaecomastia with eplerenone)

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Describe features of sacubatril/valsartn (ARNI, Entresto) (1)

Neprolysin inhibitor (ARB). Neprolysin is neutral endopeptidase in kidneys. Breaks down ANP, causes vasodilation, natriuresis and suppression of cardiac hypertrophy remodelling (ANP). Sacubatril increases ANP

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Describe features of sacubatril/valsartn (ARNI, Entresto) (2)

Neprolysin breaks down Ang II, sacubatril increases Ang II levels (effects prevented by ARB valsartan). Can be used with ARB/ACE-I in mild-moderate CHF with EF <35%

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Describe features of sacubatril/valsartn (ARNI, Entresto) (3)

Entrestro lengthens survival and reduced symptoms compared to ACE-I. Neprolysin breaks down other peptides (consequences unknown). Neprolysin breaks down b-amyloid peptide in brain (inhibition may increase risk of AD)

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Describe features of ivabradine (1)

Increased HR strongly increases risk of death in CHF. Ivabradine lowers HR by blocking I f channel in SAN, reduces CV events over 2 years with CHF (EF <35%)

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Describe features of ivabradine (2)

Possible mechanisms - reduced HR allows more time for blood to perfuse the myocardium, reducing ischaemia. Increased rate decreases cardiac contractility in CHF, reduced HR improves contractility in CHF. Reduced HR/afterload/cardiac work

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Describe features of ivabradine (3)

Adverse effects - luminous phenomena, a sensation of enhanced brightness, bradycardia

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Describe features of diuretics (1)

Furosemide. Loop diuretics (most powerful), thiazide (2nd line). Increase Na/H2O retention by kidneys, reduced CVP/oedema/dyspnoea, exercise capacity is improved when oedema is reduced

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Describe features of diuretics (2)

Side effects - K+ loss (can lead to arrhythmias). Hypokalaemia is reduced with spironolactone, ACE-I, ARBs, ENaC blockers (e.g. amiloride) or K+ supplements

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Describe features of digoxin (1)

Cardiac glycoside. Positive iontrope, increase myocyte Ca conc. by blocking Na pump, increase intracellular Na, reduces Ca extrusion by Na/Ca exchanger, symptomatic relief (no survival benefit)

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Describe features of digoxin (2)

Stimulates vagus, reduced contractility of AVN, suppress SV tachycardia (useful when CHF and AF co-exist). NICE - digoxin used for severe HR due to LVEF despite 1st/2nd line treatments

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Describe features of digoxin (3)

Narrow therapeutic window. Causes arrhythmias if myocyte Ca increases too much. Causes anorexia, nausea, vomiting. Toxicity occurs at lower doses if patient is hypokalaemic, digoxin/K+ bind to same site on Na pump

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Describe features of digoxin (4)

Toxicity treated with digibind (antibody fragment) (treat delayed after-depolarisation)

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Describe features of diastolic HF

HF with EF >40%, preserved EF. Due to stiffening of LV. Fills less during diastole, SV/CO fall even though EF is relatively preserved. Little evidence of neurohormonal antagonists/ARNI helping. Patients have diastolic/systolic CHF (treat systolic)

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Describe the treatment of acute HF (1)

Acute HF - rapid onset or worsening in/symptoms of HF. When MI compromises cardiac pumping (cardiogenic shock - organs not receiving enough blood) or when chronic HF suddenly worsens. If pulmonary oedema is present (give IV bolus of loop diuretic)

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Describe the treatment of acute HF (2)

If patient is hypoxic give O2. Opiates given to relieve anxiety and respiratory distress

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Describe the treatment of acute HF (3)

Dobutamine (increases CO) and discontinue b-blocker/vasodilator if SBP < 85 mmHg. If BP >110, use vasodilator (GTN)

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Describe features of dobutamine (1)

B1-adrenoceptor agonist, increase CO. increase cardiac work, can cause ischaemia. Can cause arrhythmias. Potentially harmful in long term, use lowest dose, for as long as necessary. Combined with dopamine - promote renal blood flow/diuresis

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Describe features of dobutamine (2)

Positive inotropic effect (b1). Newer positive inotropes such as levosimendan and relaxin are being evaluated but not mentioned in NICE guidelines

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Outline features of device therapy

Implantate cardiac defibrillators, cardiac resynchronisation therapy (implantable pacemaker), left ventricular assist devices. Resynchronise contraction of ventricles

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Organic nitrates - GTN

Lecture side - not examined

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Digoxin

Lecture side - not examined

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Pharmacology - CV Drugs 3

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