Download Pharmacological management of acute heart failure

MODULE 16:
Table 1
Cardiology
Classification of heart failure
PART 11
Pharmacological
management of
acute heart failure
New onset
First presentation acute or slow onset
Transient
Recurrent or episodic
ChronicPersistent. Stable worsening or decompensated
accounts for 80% of hospital admissions
Table 2
New York Heart Association
classification of heart failure
Class I
No limitation of physical activity. Ordinary
physical activity does not cause undue fatigue,
palpitation or dyspnoea
Class II
Slight limitation of physical activity. Comfortable
at rest but ordinary physical activity results in
fatigue, palpitation or dyspnoea
Class III
Marked limitation of physical activity.
Comfortable at rest but less than ordinary activity
causes fatigue, palpitation or dyspnoea
Class IV
Unable to carry on any physical activity without
discomfort. Symptoms at rest .If any physical
activity is undertaken discomfort is increased
by Kate O'Donovan
Heart failure is a syndrome rather than a disease entity where
patients have symptoms of breathlessness at rest or on exertion
with or without fatigue as well as signs of fluid retention (pulmonary oedema or ankle swelling). It is classified as new onset,
transient or chronic (see Table 1) and according to the patient’s
functional capacity (see Table 2). The prevalence of heart failure
is increasing because of longevity, the success in prolonging
survival in patients experiencing coronary events in addition to
postponing coronary events by effective prevention in those at
high risk or those receiving secondary prevention. Of patients
admitted to hospital with heart failure, 40% are dead or readmitted within one year with average length of hospitalisation being
nine days. The most common cause underlying this condition
in 70% of cases is coronary heart disease. Other contributing
causes include hypertension, cardiomyopathies and valvular
dysfunction (see Table 3).
The aim of this paper is to discuss the pharmacological management of acute heart failure using the ESC guidelines published
in 2008.1 Acute heart failure is defined by the guidelines as a
rapid onset or change in the signs and symptoms of heart failure,
resulting in the need for urgent therapy. It may be a first presentation or exacerbation of pre-existing chronic heart failure.
Clinical presentation will usually manifest as dyspnoea on
exertion progressing to dyspnoea at rest and/or paroxysmal nocturnal dyspnoea, signs of peripheral hypoperfusion (cold clammy
skin, hypotension, altered mentation, reduced exercise tolerance)
or as frank pulmonary oedema. The patient’s clinical status is classified using the NYHA functional classification system.
Diagnosis
Diagnosis is established based on presenting symptoms and
clinical findings as well as identifying an underlying cause that
could be treated. This comprises of a thorough history taking
and physical examination which elicits precipitating events
prior to hospital admission, such as decreasing exercise tolerance, progression of dyspnoea from exertion to rest, and
fatigue.
Physical examination may demonstrate crepes on auscultation and a third or fourth heart sound on cardiac examination
or the presence of a new murmur. A chest x ray is undertaken
as soon as feasible and may reveal cardiomegaly as well as pulmonary oedema and/or pleural effusions. An ECG is important
to out-rule or confirm the presence of ischaemia or an arrhythmia as well as providing information about heart rate, rhythm
and conduction. Bloods are reserved: full blood count (to look
for anaemia) thyroid function tests (to out rule thyroid abnormalities), arterial blood gases to assess perfusion and cardiac
biomarkers such as troponin to confirm or out rule myocardial
infarction. Natriuretic peptides such as brain natriuretic peptide
(BNP) are raised in heart failure and serve as prognostic indicators
in that the higher the level the worse the prognosis.
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Echocardiography is considered an essential diagnostic tool
as it evaluates the functional and structural changes underlying
or associated with acute presentation. The echo assesses wall
motion abnormality, valve function and pericardial effusion, as
well as estimating the ejection fraction. It is essential that this is
performed on initial assessment as it can guide patient management by identifying an underlying cause. A coronary angiogram
is indicated where an ischaemic event is suspected. Percutaneous
coronary intervention or cardiac surgery maybe indicated where
appropriate.
Management requires a well-developed treatment strategy with
realistic objectives and a plan for follow-up that should be put in
place prior to discharge. Acute phase treatment goals include alleviation of symptoms, restoration of oxygenation and peripheral
perfusion, and limiting cardiac and renal damage.
Once the patient is stabilised the treatment goals include optimising a treatment strategy, consideration of device (implantable
defibrillator or a biventricular pacemaker with/without defibrillator function) in appropriate patients and minimising hospital
stay.
Many patients require long term follow-up if the condition
progresses to a chronic state, thus it is recommended that the
patient is followed-up in a heart failure programme. Therefore,
long-term goals as described in the guidelines comprise of educating and initiating appropriate lifestyle adjustments, providing
secondary care, improving quality of life and longevity by promoting patient self-care and autonomy.
Medical management
Multiple pharmacological agents are used in the management
of heart failure but there is a scarcity of clinical trials and their use
is primarily based on expert opinion and consensus. The majority
of pharmacological agents will improve patients’ haemodynamics but have not been shown to reduce mortality.
Oxygen and morphine
It is recommended to administer oxygen as soon as possible
in hypoxic patients to achieve an oxygen saturation of > 95%
(> 90% in chronic obstructive airways disease). Care should be
taken in those with chronic obstructive airways disease to avoid
carbon dioxide retention. Initially oxygen maybe delivered via
face mask or non-breathable mask. Non-invasive ventilation (NIV)
may be used if oxygen saturation does not improve with supplemental oxygen.
This method of oxygenation refers to all modalities that assist
ventilation without the use of an endotracheal tube but with a
sealed faced mask and positive end expiratory pressure (PEEP)
such as continuous positive airway pressure and bi level positive
airway pressure. This form of pressure promotes patent alveoli
allowing for more efficient gas exchange.
NIV should be considered in those who are unable to maintain an adequate oxygen saturation to maintain peripheral
perfusion. Benefits include improved gas exchange, alleviation
of respiratory distress and improved peripheral perfusion.
The guidelines recommend early use of NIV as it reduces
the need for intubation and decreases short term mortality
risk. Intubation is restricted to patients in whom oxygen delivery is not adequate by face mask or NIV and in those with
respiratory failure/fatigue as demonstrated by carbon dioxide
retention on arterial blood gases.
Morphine is administered to alleviate restlessness, dyspnoea,
Table 3
Causes and precipitating factors
Ischaemic Heart Disease
Circulatory Failure
Acute Coronary Syndromes
Mechanical complications of
AMI
Right Ventricular Infarction
Septicaemia
Thyroidtoxicosis
Anaemia
Shunts
Tamponade
Pulmonary embolism
Valvular
Valve stenosis
Valvular regurgitation
Endocarditis
Aortic dissection
Decompensation of preexisting chronic heart failure
Lack of adherence
Volume overload
Infections especially pneumonia
Cerebrovascular insult
Surgery
Renal dysfunction
Asthma
Drug and /or alcohol abuse
Myopathies
Post partum
Acute myocarditis
Hypertension/arrhythmia
anxiety and/or chest pain associated with heart failure. Intravenous boluses of 2.5-5mg maybe administered once intravenous
access is established. It is administered with caution as it can
induce respiratory depression and cause hypotension.
Treating fluid overload
One of the mainstays in heart failure treatment is the alleviation of fluid overload using diuretics. Loop diuretics are
recommended in the acute management phase as they are
quick acting and work by increasing sodium and water loss from
the Loop of Henle in the nephron. Recommended initial dose
for moderate fluid overload is a bolus of fruisemide 20-40 mg
at admission. In cases deemed severe, or in those with a history
of chronic diuretic use, the dose may be increased according
to renal function and clinical status. Continuous infusion of
loop diuretics is considered superior in treatment compared to
boluses.
Aside from diuretics, vasodilators are recommended in the
early management in those without hypotension (systolic BP
< 90mmHg). Vasodilators improve patient symptoms and haemodynamics by reducing preload and afterload as well as improving
dyspnoea by dilating pulmonary vasculature. Intravenous nitroglycerine is the agent most commonly used.
According to the guidelines nitroglycerine may be administered as two puffs of spray under the tongue every 5-10
minutes followed by a continuous infusion. The initial infusion
dose recommended is 10-20µg /min and can be increased in
increments of 10µg/min every three to five minutes as clinical
status indicates.
The role of inotropes
Inotropes are indicated in those with low output states where
there are signs of organ hypoperfusion and congestion despite
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the administration of diuretics with or without vasodilators.
Signs of hypoperfusion include cold clammy skin, renal impairment, liver dysfunction and/or impaired mentation. Inotropes
work by stimulating the b1 receptors on the myocardium,
thus enhancing myocardial contractility. In essence inotropes
improve haemodynamics but do not positively affect mortality
or morbidity.
Two inotropic agents commonly used in clinical practice
dopamine and dobutamine. In my practice dobutamine is
more often used as it has a better safety profile compared to
dopamine. Dobutamine stimulates the b1 receptors on the myocardium, increasing contractility, with a net result of an increase
in stroke volume. The dose ranges from 2.5µg/kg/hr to 20µg/
kg/hr and maybe given peripherally. The dose is titrated according to the haemodynamic response (improved blood pressure
and signs of adequate perfusion). In those receiving b-blockers
a higher infusion rate maybe required to achieve the desired
effect.
Milrinone and enoximone are type III phosphodiesterase
inhibitors (PDEIs) and have a similar action to inotropes. Aside
from enhancing myocardial contractility they promote peripheral vasodilation. This vasodilatory effect lowers the afterload,
making it easier for the left ventricle to pump into the aorta. The
result is an increased stroke volume and cardiac output. As these
drugs do not act on the b-receptors b-blockers may be administered concomitantly. Like inotropes, milrinone and enoximone
are administered as continuous infusions but are preceded by a
bolus.
Another infusion that is used in the treatment of acute heart
failure is levosimendan. Unlike the other classes of infusions levosimendan is a calcium sensitiser that improves cardiac output
and causes vasodilation. Like the PDEIs this vasodilatory action
decreases left ventricular workload. It may be administered as
a bolus of 3-12µg/kg over 10 minutes followed by an infusion
(0.05-0.2µg/kg/min) for 24 hours.
In patients with systolic blood pressure < 100mmHg it is
recommended to start the infusion without the bolus. The
haemodynamic effect is maintained for several days after it has
been discontinued.
Vasopressors
The final class of drugs for discussion are vasopressors
(adrenaline and noradrenaline). These are reserved for those
in cardiogenic shock when the combination of an inotrope
and fluid challenge fails to restore systolic blood pressure >
90mmHg with evidence of organ hypoperfusion. They work
by causing vasoconstriction and thus increasing the blood
pressure.
Noradrenaline is recommended as the agent of choice
whereas adrenaline is reserved as a first line drug in cardiac
arrest situations. Noradrenaline maybe given concomitantly
with an inotrope but observe for excessive vasoconstriction
and the drug should be discontinued as soon as clinically
feasible.
Long-term pharmacological therapy
Once stabilised maintenance therapy is implemented. The aim
of maintenance therapy is to counteract the compensatory mechanisms involved in heart failure. When left ventricular dysfunction
is present compensatory mechanisms attempt to maintain cardiac output necessary for adequate peripheral perfusion.
The two compensatory mechanisms that are primarily targeted
are the sympathetic nervous system and the renin angiotensin
aldosterone system, which, when activated, attempts to maintain
cardiac output by increasing heart rate, causing vasoconstriction
and conserving sodium and water.
Although these mechanisms initially increase cardiac output they increase ventricular workload and in essence worsen
myocardial function. Common pharmacological therapies that
counteract these mechanisms are diuretics which target fluid
overload, b-blockers which inhibit the sympathetic nervous system and renin-angiotensin-aldosterone inhibition (ACE inhibitors,
angiotensin receptor blockers and aldosterone antagonists). It is
beyond the scope of this article to discuss maintenance therapy
in detail.
This article (part one of two) addressed the acute pharmacological management of heart failure. Goals include alleviation
of symptoms and restoration of peripheral perfusion. Part two
will discuss the nursing implications integral to the holistic care
of this patient group as well as the nursing care involved in the
acute pharmacological management.
Kate O'Donovan is course co-ordinator for the postgraduate diploma in
cardiovascular nursing in the Mater Hospital, Dublin
Reference
1. Dickstein K, Cohen-Solal A, Filippatos G. ESC guidelines for the diagnosis and treatment
of acute and chronic heart failure. 2008 Eur Heart J 2008; 29: 2388-2442
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