Heart Failure Management
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Any child in acute heart failure should be assessed for symptoms and signs of congestion and or hypoperfusion as outlined in the box. Warm and dry is the normal state of children without acute heart failure. The management for the various presentations is as follows:
Warm and Dry
These patients have compensated heart failure. Investigations can commence and treatment begun as per the Transition Care Section
Warm and Wet - Congestion without Hypoperfusion
- Fluids should be restricted to 80% of normal and a negative balance maintained
- If on β blocker therapy - stop them
- Treat any precipitating factors
- Consider anticoagulation - Enoxaparin monitored with anti-factor Xa activity, targeting a level of 0.5 - 1.0 IU/ml
- Initiate or up titrate diuretics. If the patient is not already on diuretics, start intravenous furosemide. If they are already on diuretic treatment double the home treatment dose
- If furosemide is not effective additional thiazide diuretics may be given - oral hydrochlorothiazide or intravenous chlorothiazide or oral metolazone
- If there is no response to diuretic therapy after 48-72 hours or the patient is deteriorating, start milrinone and if further escalation required commence dopamine/dobutamine or levosimendan
- Arrhythmias should be controlled with an amiodarone infusion
When the congestion is caused or compounded by restrictive or obstructive physiology:
- Caution is necessary regarding diuretic therapy as the cardiac output is dependent upon a high preload. Aggressive diuresis should thus be avoided and a MRA (aldosterone) is preferable to a thiazide
- If there is significant LVOTO an esmolol infusion should be commenced with a target heart rate reduction of 20%
The overall aim is to eliminate congestion and obtain a stable "dry" weight.
Cold and Wet - Congestion with Hypoperfusion
Congestion is treated as outlined for "Warm and Wet" above with the introduction or up titration of diuretics. Continuous furosemide infusion or the addition of intravenous chlorothiazide may be required. Hypoperfusion should be treated with milrinone ± dopamine/dobutamine escalating to adrenaline if necessary. Noninvasive or invasive ventilation may be required for respiratory distress.
Cold and Dry - Hypoperfusion
These patients need urgent improvement in cardiac output with adrenaline and if the diastolic pressure is low noradrenaline ± vasopressin. They need careful monitoring and may require mechanical assistance including ventilation, ECMO ± Impella support.
- Milrinone is a phosphodiesterase-3 inhibitor and prevents degradation of cAMP. cAMP is important in activating phosphorylation withing myocytes and hence contractility. Milrinone also reduces vascular resistance (pulmonary and systemic)
- Dopamine is a precursor of noradrenaline but stimulates α and β receptors in its own right and also enables norepinephrine release from the adrenal gland. It triggers dopaminergic receptors (DA1 & DA2) causing vasodilation and this effect predominates at low doses
- Dobutamine is a synthetic analogue and has similar effects to dopamine but without stimulating the α and dopaminergic receptors
- Vasopressin is produced naturally in the posterior pituitary gland when it is known as antidiuretic hormone - ADH. In physiological amounts its main action is acting on V2 receptors in the tubules enhancing water reabsorption but it also acts on V1 receptors which, when infused at higher concentrations is a potent vasoconstrictor
- Levosimendan sensitizes intra-myocyte Troponin C to the effects of calcium thereby increasing systolic contraction. This effect reduces in diastole and thus diastolic function is preserved or improved.
It is important to realize that inotropes can relieve the hemodynamic effects of heart failure by improving contractility, increasing the heart rate, and redistributing the cardiac output, but they do not address the underlying ventricular dysfunction. Indeed they may worsen ventricular dysfunction by increasing myocardial oxygen consumption, and exacerbate ischemia and arrhythmias.
Last Updated: May 2023