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Review

High output heart failureP.A. MEHTA1 and S.W. DUBREY2

From the1Clinical Cardiology, National Heart and Lung Institute, Imperial College, Dovehouse Street,

London SW3 6LY, UK and 2Cardiology Department, The Hillingdon Hospital, Pield Heath Road,

Uxbridge, Middlesex, London UB8 3NN, UK

Summary

The symptoms and signs of heart failure can occurin the setting of an increased cardiac output and hasbeen termed high output heart failure. An elevatedcardiac output with clinical heart failure is associatedwith several diseases including chronic anaemia,systemic arterio-venous fistulae, sepsis, hypercapniaand hyperthyroidism. The underlying primary phys-iological problem is of reduced systemic vascularresistance either due to arterio-venous shunting orperipheral vasodilatation. Both scenarios can lead toa fall in systemic arterial blood pressure andneurohormonal activation leading to overt clinicalheart failure. In contrast to low output heart failure,

clinical trial data in this area are lacking. The use ofconventional therapies for heart failure, such asangiotensin converting enzyme inhibitors, angioten-sin receptor blockers and certain b-blockers withvasodilatory properties, is likely to further reducesystemic vascular resistance resulting in deteriora-tion. The condition, although uncommon, is oftenassociated with a potentially correctable aetiology.In the absence of a remediable cause, therapeuticoptions are very limited but include dietary restric-tion of salt and water combined with judicious use ofdiuretics. Vasodilators and b-adrenoceptor positiveinotropes are not recommended.

IntroductionThe syndrome of heart failure is a global clinical

problem with at least 10 million patients across

Europe1 and 5 million in the USA2 living with

the condition. The condition is not confined to the

developed world. In the developing world, the

epidemiology of heart failure is largely unknown

but is likely to evolve in a similar way due toWesternization of lifestyle and better control of

communicable disease and malnutrition.3,4

Heart failure is usually associated with a lowcardiac output but less commonly the symptoms

and signs of heart failure can occur in the setting of a

high cardiac output. Historically this has been

termed high output heart failure.

Low output cardiac failure is well described with

a number of pharmacological therapies availablewhich are supported by data from many randomized

clinical trials.514 In addition, several internationalconsensus guidelines are available for the diagnosis

and management of heart failure.1,15 However, such

clinical evidence and published guidelines do notmake reference to high output heart failure.

Definition of high output cardiacstate and heart failureA high cardiac output has been described as being

>8 l/min or a cardiac index >3.9 l/min/m2.16 A high

Address correspondence to P.A. Mehta, Clinical Cardiology, National Heart and Lung Institute, ImperialCollege, Dovehouse Street, London SW3 6LY, UK. email: [email protected]

! The Author 2008. Published by Oxford University Press on behalf of the Association of Physicians.All rights reserved. For Permissions, please email: [email protected]

Q J Med2009;102:235241doi:10.1093/qjmed/hcn147 Advance Access publication 5 November 2008


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cardiac output state and associated clinical heartfailure is associated with several disease states

(Figure 1). Some authors suggest the term highoutput heart failure is a misnomer as the heart isintrinsically normal and capable of generating ahigh cardiac output.16 Others have suggested thathigh output heart failure occurs only when there isthe presence of underlying heart disease.4 It is likelythat in chronic high output states, heart failureoccurs due to eventual deterioration due to thepresence, or in most cases the development of heartdisease. A persistent high output state may beassociated with ventricular dilatation and/or hyper-trophy, persistent tachycardia and functional valvu-lar abnormalities, all of which may culminate in

heart failure.

PathophysiologyThe underlying primary physiological problem inhigh output heart failure is of reduced systemicvascular resistance. This occurs due to eithersystemic arterio-venous shunting or peripheralvasodilatation. Both scenarios can lead to a fall in

systemic arterial blood pressure, a feature of lowoutput heart failure. This can lead to sympathetic

neural activation, a compensatory rise in cardiacoutput and neurohormonal activation (including thereninangiotensinaldosterone system and vaso-pressin). This process in turn can cause salt andwater retention and overt clinical heart failure. Thus,salt and water retention occur both in low and highoutput heart failure due to a similar neurohormonalresponse to arterial hypotension.1720 In the former itis due to low cardiac output and in the latter due toreduced systemic vascular resistance.

Diagnosis

Symptoms and signs

In common with low output states, patients withhigh output heart failure may have a number ofsymptoms including breathlessness at rest or onexertion, exercise intolerance, fatigue and fluidretention. The signs of typical heart failure may bepresent including tachycardia, tachypnoea, raisedjugular venous pressure, pulmonary rales, pleuraleffusion and peripheral oedema (Figure 2).

Direct

myocardial

toxicity

Reduced systemic vascular resistance

Vasodilatation

Chronic anaemia

Chronic hypercapnia

Thyrotoxicosis

Sepsis

Beriberi heart disease

Pregnancy

Obesity

Hepatic disease*

Carcinoid syndrome*

Systemic arterio-venous fistula

Pagets disease

Multiple myeloma

Albrights disease

Hepatic disease*

Carcinoid syndrome*

Increased

heart rateIncreased

vasoconstriction

Sympathetic activation

Arterio-venous shunting

Reduced arterial blood pressure

Reduced renal perfusion

RAAS activation

Interstitial fibrosisSalt and water retention

Ventricular remodelling

Clinical heart failure

RAAS-Renin-Angiotensin-Aldosterone-System

* Hepatic disease and carcinoid syndrome may

cause both vasodilatation and arterio-venousshunting

Figure 1. Schematic illustrating the two common routes through which various disease states lead to a reduced systemicvascular resistance and ultimately clinical heart failure.

236 P.A. Mehta and S.W. Dubrey


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In high output heart failure, patients are likely tohave warm rather than cold peripheries due to lowsystemic vascular resistance and peripheralvasodilatation.

Investigations

Chest radiographyA chest radiograph is essential in the investigation ofheart failure. It is useful in the assessment ofcardiomegaly, pulmonary congestion and pleuralfluid accumulation. The findings of pulmonarydisease and sepsis due to pneumonia may berelevant in the diagnosis of high output heart failure.

Echocardiography

Cardiac ultrasound is mandatory in patients withsuspected heart failure. In high output states,echocardiography may demonstrate a preserved leftventricular ejection fraction (>4550%). High outputheart failure may occur despite normal left ven-tricular systolic function. Patients may subsequentlydevelop compensatory left ventricular dilatation hypertrophy. This may have eventual deleteriousconsequences with worsening heart failure.

Venous blood gas

Invasive haemodynamic measurements in heartfailure patients are often not necessary and direct

measurement to confirm a high cardiac output maynot be available. A mixed venous oxygen saturation(SvO2) provides an estimate of the body oxygenconsumption/delivery ratio and an approximationof cardiac output and organ perfusion. A low SvO2(75%) may

be due to a high cardiac output state.

Specific conditions associated withhigh output heart failureA wide spectrum of congenital, acquired andiatrogenic conditions may cause a high outputstate and lead to the clinical syndrome of heartfailure (Figure 1). In many cases this starts as anadaptive physiology, such as in an athletesheart.2126 It is when this stimulus to change ispersistent that the adaptation can result in

reduced cardiac function. In many cases this isthe beginning of a self-perpetuating cycle ofdeterioration.

Anaemia

Severe chronic anaemia can result in physiologicaladjustment to maintain tissue perfusion and oxyge-nation.27 Anaemia can lead to peripheral vasodila-tation, at least partly due to increased renal and

Suspected diagnosis of HF

(based on history, symptoms, signs, electrocardiography, chest radiography, natriuretic peptides)

Warm peripheries

Preserved left ventricular function *Cardiac output >8L/min

Mixed venous oxygen saturation (SvO2) >70-75%

Aetiology consistent with high cardiac output state (See Figure 1)

Cool peripheriesLeft ventricular systolic dysfunction*

Significant valvular disease

Cardiac output


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vascular nitric oxide synthase activity28 and lowblood viscosity.29 Both may lead to low systemicvascular resistance with associated neurohormonalactivation and heart failure.27 Treatment is aimed atcorrection of the underlying cause of anaemia.Whilst cautious blood transfusion may be necessary,rapid blood volume expansion may worsen pul-monary oedema.

Systemic arterio-venous fistula

Systemic arterio-venous fistulae may cause highoutput heart failure30,31 due to a lowering of thesystemic vascular resistance and a compensatoryrise in cardiac output.

Acquired arterio-venous fistulae may be iatro-genic or occasionally due to trauma. The creation ofarterio-venous fistulae in renal dialysis patients hasrevealed the extent and timing of associated cardiacadaptation. This includes increase in left ventricular

dimensions and a reduction in left ventriculardiastolic filling time. An associated increasedrelease of natriuretic peptides has been observed.32

The degree of increase in cardiac output depends onthe physical size and flow magnitude of thefistula.31,33 Concomitant chronic anaemia willhave an additive effect. Treatment may necessitatereversal or modification of the shunt.

Congenital arterio-venous fistulae, such as inhepatic endotheliomas and lung and/or liver invol-vement in hereditary haemorrhagic telengiectasia(Osler-Weber-Rendu disease) may produce a hyper-dynamic circulation and subsequent heart failure as

described.3436

Arterio-venous malformations maybe in the limb with associated hypertrophy (Parkes-Weber syndrome).37,38 Heart failure has also beenreported in the setting of diffuse arterio-venousmalformations associated with KlippelTrenaunaysyndrome.39 Overall, the ideal treatment is aimed atattempting surgical excision of the causative shunt.However, lesions may be difficult to preciselylocalize or in some cases so extensive as to preventcomplete excision.

Pagets disease

Pagets disease is associated with rapid boneformation and resorption that can lead to increasedblood flow within bone and the surrounding limbtissue.40 This may act or indeed cause shunting andlower peripheral vascular resistance. Significantbony involvement (usually defined as >15%) maythen lead to heart failure.41,42 Both multiplemyeloma43,44 and fibrous dysplasia (Albrights dis-ease), by a similar mechanism have been associatedwith arterio-venous shunting and high output heart

failure. Again, concomitant anaemia is likely toexacerbate this process.

Chronic hypercapnia

Chronic hypercapnia is associated with vasodilata-tion and can potentially lead to systemic hypoten-sion and subsequent adverse neurohormonal

response.45,46 Hypercapnia is commonly seen inclinical practice due to chronic obstructive pulmon-ary disease and cor pulmonale. These conditionscan lead to fluid retention in the setting of normal/increased cardiac output.

Hyperthyroidism

Thyrotoxicosis is associated with a hyperdynamiccirculation. There can be associated tachycardia,left ventricular dilatation and increased cardiacoutput.4750 The development of heart failure maybe predominantly due to tachycardia-mediated

cardiomyopathy as observed with many othercauses of tachycardia including atrial fibril-lation.51,52

Sepsis

Sepsis and associated endotoxaemia is a complexand multifactorial process. Severe septicaemia isassociated with systemic vasodilatation and anincreased cardiac output.53,54 A number of vasoac-tive cytokines including tumour necrosis factor-a,interleukins-2, -6, -8 and -15 and inducible nitricoxide synthase have been implicated in this

process.5557 The end-result is sometimes significantsystemic vasodilatation culminating in arterialhypotension and high output failure.

Beriberi heart disease

This condition is due to severe long-term (>3months) deficiency of the B vitamin thiamine andis more common in areas of dietary deficiency withhigh carbohydrate intake (such as the Far East). Inthe developed world it is most frequently observedin chronic alcoholics due to poor dietary intake ofthiamine, impaired thiamine absorption, metabo-

lism and storage. Thiamine deficiency is alsoassociated with malabsorption conditions, dialysisand other causes of chronic protein-calorie under-nutrition. The latter should be suspected in isolatedelderly patients. Beriberi heart disease is a cause ofheart failure with associated elevated cardiacoutput, oedema, fatigue and general malaise (wetberiberi). High output heart failure is possibly due toarteriolar and cutaneous vasodilatation leading to areduced systemic vascular resistance.58,59



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Obesity

Obesity produces an increase in overall bloodvolume and cardiac output. This is due to theraised metabolic activity of excessive adipose tissue,which leads to compensatory cardiac changesincluding left ventricular dilatation and eccentrichypertrophy. These adaptive modifications can

eventually lead to both systolic and diastolicabnormalities culminating in heart failure or obesitycardiomyopathy.6065 Obesity cardiomyopathy islikely to become increasingly prevalent over timedue to a rising global epidemic of obesity.

Other causes

There are many other causes of high output heartfailure including pregnancy, hepatic disease andcarcinoid syndrome. All are related, via a commonmechanism, to vasodilatation and a fall in bloodpressure.

TreatmentAlthough the final pathogenesis of salt and waterretention is similar in low and high output states,treatment options differ. In low output heart failure,with associated normal or high systemic vascularresistance, circulating vasoconstrictors predominateand are counteracted by neurohormonal antagonists(angiotensin converting enzyme inhibitors, angio-tensin receptor blockers, aldosterone antagonistsandb-blockers). Extensive clinical trial data support

the use of such therapies with improvement inmortality and morbidity.514

The evidence base for the management of highoutput failure is scarce and generally based on casereports. Clinical trial data in this area are lacking.The use of established vasodilator therapies, such asangiotensin converting enzyme inhibitors, angioten-sin receptor blockers and some newer b-blockerswith vasodilatory properties (e.g. carvedilol, nebi-volol), in patients with low systemic vascularresistance in high output heart failure is likely tolead to further deterioration and is not recom-mended. In addition the use of b-adrenoceptor

positive inotropes is not advisable.Treatment should be targeted at correcting the

cause of low systemic vascular resistance. Inaddition dietary restriction of salt and water andjudicious use of diuretics is advised. Althoughtreatment options are limited for high output heartfailure, there are some existing supportive therapies.A number of intravenous vasoconstrictor adren-ergic drugs are available including noradrenaline,ephedrine, metaraminol and phenylephrine.

These treatments increase systemic vascular resis-tance by acting on a-adrenergic receptors toconstrict peripheral blood vessels. Such therapiesmay be useful short-term adjuncts in high outputheart failure whilst treatment of the underlyingaetiology is ongoing. Long-term treatment may beassociated with both reduced vital organ perfusionand tachycardia due to b-adrenergic receptoractivation (e.g. ephedrine) and is not recommended.Respiratory intervention with high ventilatory peakend-expiratory pressure for resistant pulmonaryoedema may also be useful.

ConclusionMany conditions are associated with high cardiacoutput physiology. When this becomes chronic theadaptive cardiac changes can fail, resulting incardiovascular decompensation. Overt high outputheart failure, although uncommon, is often asso-ciated with a potentially correctable aetiology.There is a notable lack of clinical trial data for thispoorly understood condition. In the absence of aremediable cause, therapeutic options are limited.Moreover, many accepted therapies for low outputheart failure are in fact contra-indicated.

Conflict of interest: None declared.

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