EXACERBATION OF CONGESTIVE CARDIAC FAILURE
“The Dropsical Woman”, oil on wood, Gerrit Dou, 1663, Musée du Louvre, Paris, France
“…Mr. Harrison took four draughts of the foxglove, vomited a little and then purged twenty times with great debility; had next day but one a violent inflammation of the liver with much Pain…
…Mrs. -----, was asthmatic and dropsical, but did not appear near her end. She took four drafts of the decoction of foxglove. She vomited two or three times and then purged twice and died…”
Medical Case notes of Dr Erasmus Darwin, 1776.
The symptoms of heart failure had been well recognized by the medical profession for centuries as demonstrated by the Seventeenth century Dutch painter Gerrit Dou’s “The Dropsical Woman”. The exact cause, let alone how to treat the condition, remained a complete mystery however until the brilliant discovery by Dr. William Withering in the late Eighteenth century, of digitalis. He was able to deduce that it was “foxglove” that was the beneficial agent of a secret local herbal remedy that appeared to be beneficial in certain types of “dropsy”. Withering was a close friend of Dr Erasmus Darwin, (the grandfather of Charles) and both men were children of the “Enlightenment” anxious to embrace the new scientific revolutions of their time. He discussed his findings with Darwin of the beneficial effects of foxglove in patients suffering from “the dropsy”. Darwin was so impressed by Withering’s results that he enthusiastically took up the new treatment. His initial results however were somewhat disheartening to say the least as can be judged from some of his medical case reports from that time. Withering maintained that Darwin and others with similar disheartening results were not properly experienced in the use of the new drug and were using incorrect dosages and that it was not appropriate for all types of “dropsy”. As he recognised that the “concoction” acted on the heart, he deduced that it would only be of benefit in dropsy that was a result of heart disease. Experimental medicines, he cautioned his colleagues could kill as well as cure if not used in an appropriate manner.
Little further advancement was made in the treatment of heart failure over the ensuing two centuries until late in the 20th century when the understanding of the pathophysiology of cardiac failure had progressed to the point that enabled the development new classes of drugs such diuretics and agents capable of reversing the basic pathophysiologic processes of cardiac failure, such as the ACE inhibitors and beta-blockers.
Now in the 21st century with wondrous advances in technology we stand poised to take the next new steps in the treatment of dropsy, (of the cardiac variety). Unlike in Withering’s or Darwin’s day we now have an impressive array of new investigative modalities that allow us for the first in history to a make precise diagnoses of the cause and to objectively assess the severity of our patient’s “dropsy”. New technologies include devices that optimize the efficient functioning of the heart that would have astounded even the most “enlightened” men of the Seventeenth century such as Withering and Darwin.
EXACERBATION OF CONGESTIVE CARDIAC FAILURE
Introduction
Exacerbation of chronic congestive cardiac failure is a very common presentation to the Emergency Department.
This condition should be distinguished from what most Emergency physicians and Intensivists call acute cardiogenic pulmonary edema, which presents as a sudden onset of severe dyspnea, where the patient is hypoxic and acutely very unwell. American terminology sometimes refers to “flash pulmonary edema”. This condition represents a different pathology to “exacerbation of chronic congestive cardiac failure” and treatment approaches are different, (see separate guidelines for acute cardiogenic pulmonary edema).
Whilst acute cardiogenic pulmonary edema is primarily a problem of fluid maldistribution, exacerbation of congestive cardiac failure is primarily one of fluid overload.
Important aspects of management in exacerbation of heart failure include:
●An assessment of the degree of disability of the patient and how this differs from their usual functioning.
●Treatment of patient’s symptoms
● Excluding or treating any underlying causative pathology and/ or precipitating event.
It should be noted that heart failure is a symptom rather than a disease in itself, and as such an underlying cause should always be sought and treated where possible.
Epidemiology
Chronic heart failure is a progressive disease mostly affecting people over the age of 65 years.
The prevalence increases markedly with age, affecting about 1 % of people 50-59 and over 10 % of those over 80 years.
Physiology
The normal physiological determinants of the cardiac output can be summarised as below:
VR = msfp-RAP
TPR
Preload Contractility Afterload
HR SV
CO TPR
BP
VR= venous return, RAP= right atrial pressure, msfp= mean systemic filling pressure, HR= heart rate, SV=stroke volume, CO= cardiac output, TPR= total peripheral resistance, BP= blood pressure.
Pathophysiology
In heart failure there is an inadequate cardiac output for the requirements of the tissues.
Three main adaptations occur in heart failure:
●The Frank-Starling response to an increased preload
●Myocardial hypertrophy
●Activation of neurohumoral systems.
As heart failure progresses these mechanisms become maladaptive and treatment aims to restore a balance.
Heart function is generally measured by;
1.Ejection fraction:
●This is stroke volume/ end diastolic volume, (normally around 70/120 mls or approximately 0.6)
2.Cardiac index:
●This is the cardiac output per square meter of body surface area.
Causes of heart failure
The general term cardiomyopathy is often applied to the failing heart.
The term primary cardiomyopathy is generally applied when the aetiology is unknown and secondary cardiomyopathy when the aetiology is known.
The principle known causes of heart failure include
1.Ischemic heart disease, due to coronary artery disease.
2.Hypertensive cardiac disease.
3.Valvular heart disease.
4.Post infectious:
●This is usually considered to be a post-viral dilated cardiomyopathy.
5.Anaemia
6.Cor pulmonale:
●Right heart failure secondary to severe chronic lung disease.
Less common causes include:
7.Hypertrophic cardiomyopathy
8.Metabolic:
●Thiamine deficiency
●Thyroid toxicity or failure
9.Toxic:
●Alcohol
●Cardiotoxic drugs
●Chemical poisons
10.Chronic constrictive pericarditis
Classification of heart failure:
In general pathological terms heart failure can be:
1.Systolic heart failure, (most commonly)
●This is usually seen as a congestive or dilated cardiomyopathy.
2.Diastolic heart failure:
●Included in this group are hypertrophic cardiomyopathies and restrictive cardiomyopathies.
●Pure isolated diastolic failure is relatively uncommon.
3.Combination of systolic and diastolic heart failure:
●Many cases of systolic failure will also have some degree of associated diastolic failure.
Heart failure is generally a consequence of myocardial damage leading to impaired systolic function.
However, some patients, particularly the elderly and patients with hypertension or diabetes, present with classical symptoms and signs of heart failure but investigation reveals normal or near-normal systolic function (ejection fraction greater than 40%).
In these cases there are two possibilities:
The patient does not have heart failure (consider fluid overload, renal failure, severe lung disease, pericardial effusion, pericardial constriction).
The patient has principally diastolic heart failure. Here there is a failure of adequate diastolic relaxation. There are some differences in how management is approached in patients with diastolic heart failure.
Both systolic and diastolic heart failure result in a decrease in stroke volume.
Causes of exacerbation of heart failure
Regardless of the specific underlying cause, heart failure may have a precipitating or aggravating factor requiring specific therapy.
Precipitating factors may include:
1.Acute coronary syndrome
2.Arrhythmias
3.Infection
4.Medication related:
Non-compliance with medication
Or
Inadequate medical treatment
Or
Drug therapy exacerbating heart failure, including:
●Negatively inotropic drugs (eg verapamil, diltiazem, in particular)
●Salt-retaining drugs (eg corticosteroids, non-steroidal anti-inflammatory drugs, including COX-2 inhibitors)
5.Fluid overload
6.Anaemia
7.Pulmonary emboli, (worsening right heart failure).
8.Hyperthyroidism
9.Acute valvular dysfunction
Clinical Assessment
Important points of history:
The “classical” features of heart failure on history include:
1.Exertional dyspnea:
●This is the first sign of heart failure.
●As the severity of heart failure increases, dyspnea occurs at decreasing levels of activity
2.Orthopnea:
●Dyspnea that develops as soon as the patient assumes a recumbent position.
●It is usually relived promptly once the patient sits upright
3.Paroxysmal nocturnal dyspnea:
●Here there is sudden awakening from sleep with breathlessness.
●In contrast to orthopnea, which may be relieved immediately by sitting up in bed, attacks of paroxysmal nocturnal dyspnea may require 30 minutes or longer in this position for relief.
This is in distinction to acute cardiogenic pulmonary edema, where the patient develops life threatening symptoms that do not resolve spontaneously, and requires timely medical intervention for survival.
Important points of examination:
1.Vital signs:
●Including the SaO2 on pulse oximetry
●There will usually be resting tachycardia.
●Pulsus alternans may be detected.
2.Heart sounds: S3 “gallop”:
●Despite its apparent textbook importance, this is a subtle, non-specific and subjective sign that held more relevance in the pre-echocardiography era.
Heart failure may be left ventricular or right ventricular, however usually both coexist in the syndrome of congestive, or biventricular, heart failure.
3.Evidence of LVF:
●Basal lung crepitations.
4.Evidence of RVF:
●Elevated JVP.
●Hepatomegaly.
●Ascites.
●Pitting leg edema.
Classification of the severity of heart failure:
This is most commonly graded according to the New York Heart Association Functional Classification of Heart Failure, as follows:
Class 1
●Patients with cardiac disease but without resulting limitation of physical activity.
●Ordinary physical activity does not cause undue fatigue, palpitation, dyspnea, or anginal pain.
Class II
●Patients with cardiac disease resulting in slight limitation of physical activity.
●They are comfortable at rest. Ordinary physical activity results in fatigue, palpitation, dyspnea, or anginal pain.
Class III
●Patients with cardiac disease resulting in marked limitation of physical activity.
●They are comfortable at rest. Less than ordinary activity causes fatigue, palpitation, dyspnea, or anginal pain.
Class IV
●Patients with cardiac disease resulting in inability to carry on any physical activity without discomfort.
●Symptoms of heart failure or the anginal syndrome may be present even at rest. If any physical activity is undertaken, discomfort is increased.
Investigations
The extent of investigation required in the patient who presents with an exacerbation of heart failure will depend on how unwell the patient is and the index of suspicion for any given causative or aggravating pathology
The following may be considered:
Blood tests
1.FBE:
●Haemoglobin level, for anaemia.
●Elevated WCC as evidence of possible infective process
2.U&Es/ eGFR
●Chronic severe heart failure can lead to impaired renal function.
3.Glucose level
4.CRP
5.Cardiac enzymes
●ACS is a common cause of exacerbation of CCF.
6.BNP:
●This correlates well with the degree of heart failure. Its level correlates closely with the NYHA Classification of Heart Failure.
●If values are normal it makes a diagnosis of heart failure unlikely, and an alternate cause for symptoms will need to be considered.
Others tests may be done as clinically indicated:
6.ABGs
7.Blood cultures
8.Thyroid function tests
9.LFTs:
●Chronic severe heart failure can lead to impaired liver function.
ECG:
This should be done in all cases, in particular looking for:
●Arrhythmias
●Evidence if ischemia
CXR:
A CXR should done, in particular looking for:
●Signs of congestive heart failure:
Note that the radiographic signs of heart failure may lag behind the clinical picture, and may be relatively slower to resolve with respect to the clinical picture.
Radiographic signs of heart failure include:
♥Upper lobe blood diversion is usually the first radiographic sign of heart failure.
♥Interstitial edema, this is represented as fine linear opacities; (peripherally placed basal ones are termed Kerly B lines, whilst more central ones are termed Kerly A lines).
♥Cardiomegaly, (a subjective and variable sign however).
The acute onset of bilateral or unilateral “fluffy” alveolar edema (commonly termed “bats wings”) is characteristic of acute cardiogenic pulmonary edema.
●An alternate diagnosis (such as consolidation).
Echocardiography:
An echocardiogram should be done in all cases presenting as a new clinical diagnosis of heart failure, in order to make an objective and definitive diagnosis.
It will also document the degree and type of failure, and may diagnose an underlying causative pathology, (such as valvular heart disease).
Echocardiography is also useful in established cases to document disease progression.
Nuclear medicine imaging:
Radionuclide multiple gated acquisition (MUGA) scan is a very reliable imaging technique for determining global heart function.
LV ejection fraction, as determined by MUGA scanning, is often used for serial assessment of LV function because of its reliability.
Coronary angiography:
In selected cases coronary angiography may be needed to document the contribution and degree of coronary artery disease, as well as its suitability for intervention.
Management
Management issues in the ED will include:
1.Oxygenation:
●Oxygenation is the immediate priority for any patient who presents to the Emergency Department acutely short of breath.
●Patients should be sat upright as much as possible and given oxygen therapy as required.
2.Attention to any underlying cause or precipitating factors:
●An underlying precipitating factor (such an ACS, anaemia or infection) should always be sought and treated as required.
Ongoing ward management (of systolic failure) will then consist of:
3.Dietary measures:
Fluid restriction:
●In patients with severe heart failure, the ability to excrete a free water load is diminished.
●The combination of reduced sodium intake, potent diuretics and continued fluid intake often leads to dilutional hyponatraemia.
●Increasing salt intake and reducing diuretic dosage are usually inappropriate, as these patients are often still oedematous.
●Fluid intake should be limited to 1.5liters per day or less in patients with hyponatraemia, particularly in those in whom the serum sodium concentration falls below 130mmol/L.
Sodium restriction:
●The use of diuretics in heart failure patients will often avoid the need for strict sodium restriction.
●Excessive salt ingestion should be avoided however as this can precipitate or exacerbate heart failure. A no-added-salt diet restricted to 60to 100mmol per day should be adhered to.
●More severe salt restriction may be necessary in patients with severe heart failure, and a dietitian referral made.
4.Anti-heart failure drugs:
Drug therapies that have been shown to improve survival in heart failure include:
●Angiotensin converting enzyme (ACE) inhibitors
●Angiotensin II receptor antagonists
●Beta-blockers
●Aldosterone antagonists (eg spironolactone, eplerenone).
There is now a good body of evidence to support the use of combination drug therapy in heart failure to improve prognosis, and control symptoms and signs.
Almost all patients with clinical heart failure will require combination therapy with an ACE inhibitor, a beta blocker, and a diuretic.
Optimization of therapy may take several months and requires close monitoring of symptoms, fluid status, renal function and electrolyte levels to get the right balance.
For full prescribing details of anti-heart failure drugs, see the latest edition of Cardiovascular Therapeutic Guidelines.
Note however that the initiation and revision of these agents is not normally a function of the Emergency Department setting, (other than identifying possible aggravating agents). The following notes are intended merely as an informative overview on the medications that heart failure patients may be on when they present to the ED.
The focus of the ED will be the initial emergency stabilization of the patient and their immediate diagnostic workup as well as formulating an appropriate disposition plan.
General principles for these agents are as follows:
Angiotensin converting enzyme (ACE) inhibitors:
●ACE inhibitors are now considered the first line therapy for heart failure.
ACE inhibitors reduce mortality and morbidity at any grade of systolic heart failure, even in patients with asymptomatic disease and so virtually all patients with clinical heart failure should receive an angiotensin converting enzyme (ACE) inhibitor as initial therapy.
●Asymptomatic patients should receive an ACE inhibitor if there is significant left ventricular dysfunction (ie left ventricular ejection fraction less than 40%).
Angiotensin II receptor antagonists:
●Some patients are unable to tolerate angiotensin converting enzyme (ACE) inhibitors because of adverse effects such as cough or skin rashes.
●In these patients, the angiotensin II receptor blockers should be used to provide an alternative mechanism of inhibiting the renin-angiotensin system.
●However, if a patient has experienced angioedema with an ACE inhibitor, angiotensin II receptor blockers are generally contraindicated.
●Addition of an angiotensin II receptor blocker to background combined therapy including an ACE inhibitor should be considered if the patient remains symptomatic.
Beta-blockers:
Clinical trials have demonstrated the unequivocally beneficial effects of some (heart failure specific) beta blockers in patients with systolic heart failure and low ejection fraction. They show improved control of heart failure, improved left ventricular ejection fraction, and improved prognosis.
Heart failure specific beta-blockers include metoprolol, carvedilol and bisoprolol.
Patients with heart failure however are often very sensitive to beta blockers. Major complications of beta-blocker therapy in patients with heart failure include worsening of heart failure, severe hypotension and bradyarrhythmias. These complications are due to beta blockade leading to withdrawal of sympathetic nervous system support for the failing heart.