Heart failure Flashcards

Question

Management of acute HF

Answer 1

o No beta-blockers, only given in chronic HF when tachycardic o Oxygen reservoir o GBT: dilates vessels to reduce pulmonary oedema o Diuretics o Morphine o Dobutamine: positive inotropes to increase heart function o CPAP o Dobutamine/CPAP fixes low BP without using IV bolus and maintains oxygen

Answer 2

Acute medical emergency Sit patient up to reduce pulmonary congestion ``` Give oxygen (high-flow, high-concentration) - Non-invasive positive pressure ventilation (continuous positive airways pressure (CPAP) of 5–10 mmHg) by a tight-fitting facemask ``` Administer nitrates - IV glyceryl trinitrate (10–200 μg/min or buccal glyceryl trinitrate 2–5 mg, titrated upwards every 10 minutes) - Until clinical improvement occurs or systolic BP falls to less than 110 mmHg.   Administer loop diuretic, such as furosemide (50–100 mg IV).   Patient should initially be kept rested, with continuous monitoring of cardiac rhythm, BP and pulse oximetry. IV opiates must be used sparingly in distressed patients - May cause respiratory depression and exacerbation of hypoxaemia and hypercapnia. - If ineffective → inotropic agents may be required to augment cardiac output, particularly in hypotensive patients. Insertion of an intra-aortic balloon pump may be beneficial in patients with acute cardiogenic pulmonary oedema and shock.  

Answer 3

patients with high end-diastolic filling pressures and evidence of pulmonary of systemic venous congestion

Answer 4

Signs/symptoms of low cardiac output

Answer 5

• Increase in urinary Na & water excretion → reduce blood and plasma volume • Reduces preload • Improves pulmonary and systemic venous congestion. • May also reduce afterload and ventricular volume → fall in ventricular wall tension & increased cardiac efficiency. • Fall in preload (ventricular filling pressure) tends to reduce cardiac output, BUT ‘Starling curve’ in heart failure is flat o So there may be substantial and beneficial fall in filling pressure with little change in cardiac output o Excessive diuretic therapy may cause undesirable fall in cardiac output, especially in patients with marked diastolic component to their heart failure. This leads to hypotension, lethargy and renal failure. • In some patients with severe chronic heart failure, particularly if there is associated renal impairment, oedema may persist, despite oral loop diuretic therapy. o IV infusion of furosemide (5–10 mg/hr) may initiate diuresis. o Combining loop diuretic with thiazide diuretic (e.g. bendroflumethia- zide 5 mg daily) may be effective, but can cause excessive diuresis. • Mineralocorticoid receptor antagonists o Spironolactone and eplerenone → potassium-sparing diuretics that o Good in patients with heart failure with severe left ventricular systolic dysfunction. o May cause hyperkalaemia, especially if used with ACE inhibitor. o Improve longterm clinical outcome in patients with severe heart failure or heart failure following acute MI.

Answer 6

• Preventing the conversion of angiotensin I to angiotensin II → prevent peripheral vasoconstriction, activation of SNS, and salt and water retention due to aldosterone release. • Also prevent undesirable activation of RAAS caused by diuretic therapy. • Moderate/severe heart failure o ACE inhibitors - improvement in effort tolerance and in mortality, outcome and prevent onset of overt heart failure in patients with poor residual left ventricular function following MI • Can cause symptomatic hypotension and impairment of renal function, especially in patients with bilateral renal artery stenosis or those with pre- existing renal disease. • An increase in serum K concentration may occur that can offset hypokalaemia associated with loop diuretic therapy. • Short-acting ACE inhibitors can cause marked falls in BP, particularly in elderly or when started in the presence of hypotension, hypovolaemia or hyponatraemia. • Stable patients without hypotension (systolic BP > 100 mmHg), ACE inhibitors can usually be safely started in community. • Inother patients, usually withhold diuretics for 24 hours before starting treatment with a small dose of a long-acting agent, preferably given at night • Renal function and serum potassium must be monitored and should be checked 1–2 weeks after starting therapy.

Answer 7

* Block action of angiotensin II on heart, peripheral vasculature and kidney. * Heart failure - produce beneficial haemodynamic changes similar to effects of ACE inhibitors but generally better tolerated. * Comparable effects on mortality and useful alternative for patients who cannot tolerate ACE inhibitors * Have serious SE like ACEi - renal dysfunction and hyperkalaemia. * Normally used as alternative to ACE inhibitors, but can be combined in patients with resistant or recurrent heart failure.

Answer 8

* Use: chronic heart failure, when ACE inhibitor or ARB drugs are contraindicated (e.g. in severe renal failure). * Venodilators – e.g. nitrates- reduce preload * Arterial dilators – e.g. hydralazine - reduce afterload * Use limited by pharmacological tolerance and hypotension

Answer 9

* Counteract deleterious effects of enhanced sympathetic stimulation and reduces risk of arrhythmias and sudden death. * When initiated in standard doses, may precipitate acute-on-chronic heart failure * When given in small incremental doses (e.g. bisoprolol started at a dose of 1.25 mg daily, and increased gradually over a 12-week period to a target maintenance dose of 10 mg daily), can increase ejection fraction, improve symptoms, reduce frequency of hospitalisation and reduce mortality in patients with chronic heart failure * More effective at reducing mortality than ACEi: relative risk reduction of 33% versus 20%, respectively.

Answer 10

* Acts on If inward current in SA node → reduce HR * Reduces hospital admission and mortality rates in patients with HF due to moderate or severe left ventricular systolic impairment. * Best results in those with high HR (>77/min) →best suited to patients who cannot take β-blockers or in whom HR remains high despite β-blockade. * Ineffective in patients in atrial fibrillation.

Answer 11

* Provide rate control in patients with HR and atrial fibrillation * In severe heart failure (NYHA class III–IV) - reduces likelihood of hospitalisation for HF, although has no effect on long-term survival.

Answer 12

* Potent anti-arrhythmic drug - little negative inotropic effect * Use: patients with poor left ventricular function. * Only effective in treatment of symptomatic arrhythmias, * Should not be used as preventative agent in asymptomatic patients.