3.5 Preventing and Treating Acute Exacerbations of Chronic Heart Failure

Acute Heart Failure 

Patients with acute heart failure will present as medical emergencies.

Associated cardiogenic shock and/or acute respiratory failure will need to be identified and managed urgently.

Most patients who present with acute heart failure are having an acute exacerbation or decompensation of their chronic heart failure, which is what we’ve focussed on up until now.

Other patients with acute heart failure may be simultaneously suffering from an acute coronary syndrome, hypertensive crisis, dysrhythmia, major structural damage to the heart muscle or valves, or a pulmonary embolism.

Causes of Acute Exacerbations of Chronic Heart Failure

Medications that can Exacerbate Chronic Heart Failure

Various medications for a variety of different indications can cause or exacerbate heart failure.

These include the non-dihydropyridine calcium channel blockers, verapamil and diltiazem. These can further depress myocardial function in patients with heart failure and must never be used in combination with beta blockers.

Beta blockers, as we said earlier, should not be used in patients with heart failure unless they are clinically stable and not commenced until there are no signs of congestion. If the patient does start to develop signs of a mild heart failure exacerbation, then the beta blocker might be continued while we increase the diuretic dose, but if it is a more serious heart failure exacerbation then the beta blocker should certainly be stopped as it will antagonise the effects of the drugs used to treat a severe acute heart failure exacerbations.

Non-steroidal anti-inflammatory drugs (NSAIDs) are another really important group of drugs to avoid in heart failure, because they can commonly cause sodium and water retention.

Other medications that can exacerbate heart failure are listed below:

Diuretics in Acute Heart Failure

First line pharmacological therapy in acute heart failure is intravenous furosemide, to relieve signs and symptoms of congestion. Remember these include pulmonary congestion, peripheral oedema, hepatic congestion, and ascites.

The intravenous route is needed because there are often absorption issues associated with the oral route, including gastrointestinal hypoperfusion and oedema round the bowel as well.

The IV route also enables a much faster onset of action.

Since diuretics can cause blood pressure to decrease, we must ensure that the patient is maintaining adequate tissue perfusion and that their blood pressure is holding stable before giving the diuretic. We should also consider the dose. If a patient has developed fluid overload because of acute heart failure despite a regular oral diuretic dose, then we know there will be no point giving an IV dose that is equivalent to less than their oral dose. It must be at least equivalent, in most cases it will be increased.

So it is important that you remember that the oral bioavailability of furosemide is about 50%. Meaning 20mg IV furosemide is about equivalent to 50mg of oral furosemide. This is also important to remember when it comes time to switch back to oral dosing from IV dosing.

Intravenous Vasodilators 

Intravenous vasodilators, such as a continuous glyceryl trinitrate infusion or a sodium nitroprusside infusion, may be considered in patients with acute heart failure if their systolic blood pressure is greater than 90mmHg.

The rationale is to relieve symptoms of congestion by optimising preload and reducing afterload to hopefully increase stroke volume. But there is only low quality evidence to support their use as part of the treatment of acute heart failure in practice.

There is a very high risk of lowering blood pressure too low, so blood pressure is something that must be monitored very closely if intravenous vasodilators are being considered.

Patients receiving intravenous vasodilator therapy will be admitted to a high dependency unit such as the coronary care unit or intensive care unit, where there are facilities and nurse-patient ratios that can facilitate the high level monitoring that is required.

Generally, if an intravenous vasodilator is going to be used, glyceryl trinitrate will be chosen, because there are more issues associated with sodium nitroprusside, including a greater risk of lowering BP too dramatically. Sodium nitroprusside can also be associated with rebound hypertension if it is stopped too quickly.

Inotropic Therapy

Beta blockers must be ceased whenever inotropes are required.

Hopefully, you are starting to understand the rationale for these treatments and understand that the goal is to maintain cardiac output and tissue perfusion. Ideally, we achieve this by using an inotrope with vasodilatory activity (e.g., dobutamine).

But if this doesn’t work, then we can consider one with vasopressor activity to help increase blood pressure a little but not so much that increased afterload reduces the ejection fraction even more.

Extra caution should be used with inotropes that have vasopressor activity (those being dopamine, noradrenaline, and adrenaline) as vasopressor activity means increased afterload which can further reduce ejection fraction and tissue perfusion.