Diuretic therapy in chronic heart failure: Implications for heart failure nurse specialists

11
Australian Critical Care Diuretic therapy in chronic implications for heart failure heart iluFse failure: specialists Patricia Davidson ° RN ITC BA MEd MRCNA Associate Professor of Nursing ' Clinical Nurse Consultant (Cardiology)2 Peter Macdonald ° MBBS FRACP PhD Associate Professor of Medicine/Staff Cardiologist 3, 4 Glenn Paull • RN CCU Cert BN (Hans) Clinical Nurse Consultant (Heart Failure)2 David Rees ° MBBS FRACP PhD Senior Staff Specialist, Cardiology Department 2 Laurence Howes ° MBBS FRACP PhD Professor of Clinical Pharmacology 2 Jill Cockburn ° MSc PhD s Professor of Behavioural Science in Relation to Medicine Mark Brown • MBBS, FRACP MD Professor of Medicine, Senior Staff Nephrologist 2 ' School of Nursing, Family and Community Health University of Western Sydney, NSW 2The St George Hospital, Sydney, NSW 3 University of NSW 4Heart & Lung Transplant Unit, University of NSW St Vincent's Hospital, Sydney, NSW s School of Medical Practice and Population Health The University of Newcastle, NSW Abstract: Chronic heart failure (CHF) is a syndrome precipitated by inadequate cardiac output and neurohormonal activation, leading to sodium and water retention. With increasing prevalence of CHF, heart failure nurse specialists (HFNS) are becoming involved in collaborative models of care in community and outpatient settings. Diuretic therapy in both acute and chronic heart failure is effective in relieving symptoms of congestion and improving cardiovascular hacmodyru~mics. Best practice guidelines dictate diuretics should not be used as monotherapy but serve as an adjunctive therapy to agents with demonstrated survival benefit, such as angiotensin.converting enzyme (ACE) inhibitors and beta.blocker therapy. Despite the widespread use of diuretic therapy, limited clinical trial evidence exists upon which to base treatment decisions and algorithms. This article seeks to review diuretic therapy and flexible diuretic regimes in CHF and to discuss implications for patient management and advanced nursing practice. Davidson P et al. Diuretic therapy in chronic heart failure: implications for heart failure nurse specialists. Australian Critical Care 2003; 16(2) :59-69. INTRODUCTION Chronic heart failure (CHF) is the only cardiovascular disease increasing in prevalence and engenders high rates of primary care presentations, hospitalisation and rehospitalisation in the elderly ~.3. There is evidence that exacerbations of CHF and readmissions can be prevented by a coordinated management strategy facilitated by heart failure nurse specialists (HFNS)4~. Diuretic therapy in CHF is part of the management strategy indicated to relieve symptoms of oedema and congestionL In order to assist patients to deal with this significant aspect of their heart failure management, HFNS require an understanding of the pharmacokinetics and physiological basis of diuretic therapy. NEUROHORMONAL F'ARAME1-ERS OF CHF The cardiovascular system relies upon several neuroendocrine compensatory mechanisms, including activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system to stabilise cardiac performance s. In CHF, decreased cardiac output increases sympathetic activity, resulting in high circulating levels of catecholamines, specifically norepinephrine 9. Initial, beneficial sympathetic norepinephrine-mediated effects include arterial vasoconstriction, tachycardia and increased myocardial contractility, all of which serve to maintain blood supply to vital organs, often at the expense of renal circulation ,0. Long-term sympathetic activation, however, is associated with myocyte toxicity, hypertrophy, activation of fetal gene expression, down regulation of beta-adrenergic receptors, redistribution of regional blood flow, rhythm disturbances and apoptosis (programmed cell death) 9. The latter effects contribute to the progression of heart failure and further deterioration of cardiac performance via angiotensin II (AII) mediated vasoconstriction and aldosterone induced sodium retention. The renin-angiotensin-system (RAS) is also activated in order to regulate cardiac output. Sustained activation, however, results in myocyte hypertrophy and dysfunction (remodelling), together with perpetuation of haemodynamic abnormalities. More recently, aldosterone itself has been implicated as being 'toxic' to endothelium. The major regulators of renin and hence All and aldosterone release are changes in effective renal blood flow, sodium chloride delivery into the macula densa and reduced afferent arteriole pressure %IL In CHF this process is complicated by further renin release consequent upon sympathetic nervous system activation. Figure 1 describes the pathophysiological processes involved in the progression of CHE 59 Volume 16 Number2 May2003

Transcript of Diuretic therapy in chronic heart failure: Implications for heart failure nurse specialists

Australian Critical Care

Diuretic therapy in chronic implications for heart failure

h e a r t

i luFse

failure: specialists

P a t r i c i a D a v i d s o n ° RN ITC BA MEd MRCNA

Associate Professor of Nurs ing '

Clinical Nurse Consu l t an t (Cardiology)2

Peter Macdona ld ° MBBS FRACP PhD

Associate Professor of Medicine/Staff Cardiologis t 3, 4

Glenn P a u l l • RN CCU Cert BN (Hans)

Clinical Nurse Consu l t an t (Heart Failure)2

David Rees ° MBBS FRACP PhD

Senior Staff Specialist, Card io logy D e p a r t m e n t 2

Laurence Howes ° MBBS FRACP PhD

Professor of Clinical P h a r m a c o l o g y 2

Jill C o c k b u r n ° MSc PhD s

Professor of Behav ioura l Science in Relat ion to Medicine

M a r k B r o w n • MBBS, FRACP MD

Professor of Medicine, Senior Staff Nephrologis t 2

' School of Nursing, Fami ly a n d C o m m u n i t y Heal th Universi ty of Western Sydney, NSW

2 The St George Hospital , Sydney, NSW

3 University of NSW

4 Hear t & Lung Transp lan t Unit, University of NSW St Vincent 's Hospital , Sydney, NSW

s School of Medical Practice a n d Popula t ion Heal th The University of Newcastle, NSW

Abstract: Chronic heart failure (CHF) is a syndrome precipitated by inadequate cardiac output and neurohormonal activation, leading to sodium and water retention. With increasing prevalence of CHF, heart failure nurse specialists (HFNS) are becoming involved in collaborative models of care in community and outpatient settings.

Diuretic therapy in both acute and chronic heart failure is effective in relieving symptoms of congestion and improving cardiovascular hacmodyru~mics. Best practice guidelines dictate diuretics should not be used as monotherapy but serve as an adjunctive therapy to agents with demonstrated survival benefit, such as angiotensin.converting enzyme (ACE) inhibitors and beta.blocker therapy.

Despite the widespread use of diuretic therapy, limited clinical trial evidence exists upon which to base treatment decisions and algorithms. This article seeks to review diuretic therapy and flexible diuretic regimes in CHF and to discuss implications for patient management and advanced nursing practice.

Davidson P et al. Diuretic therapy in chronic heart failure: implications for heart failure nurse specialists. Australian Critical Care 2003; 16(2) :59-69.

I N T R O D U C T I O N

Chronic heart failure (CHF) is the only cardiovascular disease increasing in prevalence and engenders high rates of primary care

presentations, hospitalisation and rehospitalisation in the elderly ~.3. There is evidence that exacerbations of CHF and readmissions can be prevented by a coordinated management strategy facilitated by

heart failure nurse specialists (HFNS)4~.

Diuretic therapy in CHF is part of the management strategy

indicated to relieve symptoms of oedema and congestionL In order to assist patients to deal with this significant aspect of their heart failure management, HFNS require an understanding of the

pharmacokinetics and physiological basis of diuretic therapy.

N E U R O H O R M O N A L F'ARAME1-ERS OF CHF

The cardiovascular system relies upon several neuroendocrine

compensatory mechanisms, including activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system to stabilise cardiac performance s. In CHF, decreased cardiac output

increases sympathetic activity, resulting in high circulating levels of catecholamines, specifically norepinephrine 9. Initial, beneficial

sympathetic norepinephrine-mediated effects include arterial

vasoconstriction, tachycardia and increased myocardial

contractility, all of which serve to maintain blood supply to vital organs, often at the expense of renal circulation ,0. Long-term sympathetic activation, however, is associated with myocyte

toxicity, hypertrophy, activation of fetal gene expression, down regulation of beta-adrenergic receptors, redistribution of regional

blood flow, rhythm disturbances and apoptosis (programmed cell death) 9. The latter effects contribute to the progression of heart

failure and further deterioration of cardiac performance via

angiotensin II (AII) mediated vasoconstriction and aldosterone induced sodium retention. The renin-angiotensin-system (RAS) is

also activated in order to regulate cardiac output. Sustained

activation, however, results in myocyte hypertrophy and dysfunction (remodelling), together with perpetuation of

haemodynamic abnormalities. More recently, aldosterone itself has

been implicated as being 'toxic' to endothelium.

The major regulators of renin and hence All and aldosterone

release are changes in effective renal blood flow, sodium chloride delivery into the macula densa and reduced afferent arteriole pressure %IL In CHF this process is complicated by further renin

release consequent upon sympathetic nervous system activation. Figure 1 describes the pathophysiological processes involved in the

progression of CHE

59 Volume 16 Number2 May2003

Austral ian Critical Care

Figure 1. Progression of CHF s'".

GHF \

./'" progression \~-..

Cardiac Neurohormonal Myocyte death remodelling activation (apoptosis)

Spherical geometry Noradrenaline Cytokine Chamber dilation RAS*, Aldosterone activation (TNF#)

ANP ̂ , BNP**, Endothelin

V V V Poor function Sodium retention Cardiac fibrosis Wall stress Vasoconstriction Hypertrophy

Mitral regurgitation Direct toxicity

* Renin angiotensin system

a Atrial natiuretic peptide

** Brain natiuretic peptide

# Tumour necrosis factor

DIURETIC THERAPY IN CHF

Diuretic therapy is important in relieving the oedematous symptoms

of CHF 7. Despite the plethora of pharmacological trials in CHF

powered to test mortality benefits, the Randomised Aldactone

Evaluation Study (RALES) is the only trial that evaluated the impact of a diuretic on mortality ,2. This randomised, controlled trial

evaluates the effect of spironolactone, an aldosterone antagonist

(spironolactone competes with aldosterone for receptor sites), on

mortality in patients with New York Heart Association (NYHA)

Class Ill-IV heart failure, already receiving an angiotensin-

converting enzyme (ACE) inhibitor and a loop diuretic. The

beneficial effects of spironolactone were thought to be mediated, not

primarily through its diuretic action but blockade of deleterious

effects of aldosterone. RALES demonstrated a 27% reduction in

mortality and a 22% reduction in the combined endpoint of non-

fiatal hospitalisation and mortality but several subsequent reports have cautioned clinicians about the risk of hyperkalaemia and acute

renal failure with this combination therapy ~.

Diuret i c a g e n t s A variety of diuretic agents are available (Table 1) and in patients with mild heart failure almost all are effective ~4. ~s. However, in severe

heart failure and within a context of multiple drug agents, diuretic

therapy is more complex. This complexity is exacerbated by renal

dysfunction and electrolyte imbalance ,6. Despite the temptation to

reduce oedematous symptoms, excessive diuresis must be avoided

because hypovolemia may reduce cardiac output, impair renal

function, cause electrolyte disturbances that precipitate arrhythmias,

exacerbate neurohormonal activation and impact quality of life by

producing weakness, lethargy and postural symptoms ]7.

Spironolactone, triamterene and amiloride are not potent diuretics

when used alone, but potentiate the actions of other agents,

particularly thiazide and loop diuretics. Loop diuretics, frusemide,

ethacrynic acid, bumetanide, given alone or with spironolactone or

triamterene, are the agents of choice in patients with severe heart

failure, refractory to other diuretics L4. End-stage CHF may require

combination of a thiazide, a loop diuretic and a potassium-sparing

diuretic ~42L There are, however, limited objective data supporting

this approach.

P h a r m a c o k i n e t i c s o f d iure t i c t h e r a p y Diuretic therapy decreases capillary wedge pressure and improves

NYHA functional class both in acute and CHE

Pharmacokinetics of loop diuretics are altered in CHF, with a

reduced peak concentration of frusemide in the urine and a

prolonged time to peak concentration 22 24. This may be overcome

by an increase in dose. In symptomatic CHF, loop diuretics are

necessary to improve symptoms of congestion, a modest increase

in urea may be tolerated to relieve symptoms of circulatory

congestion zo. Prerenal azotemia, due to decreased glomerular

filtration, is present in many patients with severe CHE A rise in

BUN and a small increase in creatinine may indicate impaired

renal function, haemodynamic instability and is a poor prognostic

sign.

Impaired renal function has also been identified as an independent predictor of hospital readmission 25. In renal failure, tubular delivery

of loop diuretics may be impaired due to decreased renal blood flow and impaired action of the proximal tubular carrier system'S. Thus, doses of loop diuretics often have to be increased to achieve sufficient drug concentrations within tubular fluid ~6

Flex ib le d iure t i c r e g i m e n s Flexible diuretic regimens are advocated in the management of CHF, and have demonstrated relief of symptoms and decreases in hospitalisations in multifaceted disease management interventions 26. An important aspect of flexible diuretic regimes is the promotion of self-management strategies by encouraging individual's monitoring and management of their condition.

As well as achieving better symptom control and prevention of crisis situations, flexible diuretic regimes potentially avoid over- diuresis (Figure 2). This is of significance in patients who do not require daily diuretics but occasionally require diuretic treatment related to dietary indiscretions or deterioration in cardiovascular function. As previously discussed, over-diuresis should be avoided, since the resultant hypovolemia may reduce cardiac output, interfere with renal function and produce profound weakness and lethargy ~6 The concept of flexible diuretic regimens have not received the scrutiny of large, randomised controlled trials. The availability of point of care testing for b-type natiuretic peptide (BNP) to assist in medication titration and help identify those patients most at risk of early readmission is a promising advance currently subject to evaluation 27.

Diure t i c r e s i s t a n c e Diuretic resistance is defined as a clinical state in which diuretic

response is diminished or lost before the therapeutic goal of relief

Common causes of diuretic from oedema has been reached 16.

resistance include:

Renal dysfunction.

Hyponatraemia.

Altered diuretic pharmacokinetics.

Compensatory mechanisms to restore arterial blood volume.

Non-compliance with medication and sodium and fluid

restriction.

Alcohol.

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Australian Critical Care

T a b l e 1. O r a l d i u r e t i c a g e n t s 7 ~4 ~5 2~.

Thiazide

diuretics

Chlorothiazide and

hydrochlorothiazide

reach their peak action in

4 hours and diuresis persists

for approximately 12 hours

Reduce the reabsorption of sodium

and chloride in the first half of the distal

convoluted tubule and a portion of the

cortical ascending limb of the loop of

Henle; as a consequence water

follows the unreabsorbed salt

Hypokalaemia

• Hyponatraemia

• Hypomagnesemia

• Hypochloraemia

• Metabolic alkalosis

• Hyperuricemia

Hyperglycemia

• Skin rashes

Impotence

Thrombocytopenia, granulocytopenia

Metolazone

(currently not

available

in Australia)

Thiazide

Quinethazone derivative

Usual dose 2.5-5mg/day

Effective in the

presence of moderate

renal failure

In patients with impaired renal function,

the natriuretic action of metolazone is

preserved. Given in a dose of 2.5 or 5mg

one hour before frusemide can enhance

diuresis in frusemide resistant patients

Hypokalaemia, particularly in

combination with loop diuretics

Hypotension

Hyperuricaemia

Loop

diuretics

Frusemide, bumetanide,

ethacrynic acid, piretanide

and torsemide

• Frusemide has an

onset within 30-60

minutes, with a peak

effect at 1-2 hours

and a maximum

effect of 6-8 hours.

• One milligram of

bumetanide is equivalent

to 40mg of frusemide

Inhibit the reabsorption of sodium,

potassium and chloride in the thick

ascending limb of Henle's loop

by blocking a cotransport system

in the luminal membrane

• Metabolic alkalosis

• Hypokalemia

• Hypochloraemia

Hyponatraemia

• Hyperuricemia

Hyperglycemia

• Weakness, nausea and dizziness

• Ethacrynic acid and frusemide has

been associated with transient or

even permanent deafness or

vertigo as well as with skin

rash and granulocytopenia

Aldosterone

antagonists

Spironolactone Act on the distal half of the convoluted

tubule and the cortical portion of the

collecting duct by competitive inhibition

of aldosterone, thereby blocking the

exchange between sodium and both

potassium and hydrogen in the distal

tubules and collecting ducts.

Onset of action usually requires 3-4 days.

Benefits in CHF related to aldosterone

blockade and prevention of fibrosis

• Contraindicated in patients

with hyperkalaemia, renal

failure, or hyponatraemia

• Nausea, epigastric distress

mental confusion, drowsiness,

• Gynecomastia

• Erythematous eruptions

Potassium

sparing

Triamterene and amiloride Block sodium reabsorption and

secondarily inhibit potassium secretion

in the late distal convoluted tubule

and the collecting duct

• Nausea, vomiting, diarrhoea

• Headache, granulocytopenia,

eosinophilia,

• Skin rash

• Should not be used in patients with

impaired renal function

• Hyperkalemia

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Figure 2. Guidelines for flexible diure t ic t i t ra t ion 26 (dosing recommendations based on expert opinion (Macdonald, Brown, Howes).

Guidelines for flexible diuretic regimes: these steps are to be made taking note of renal function and

haemodynamic status

Following a weight increase of > 2 kilograms (kgs)

Patients n o t o n daily diuretic therapy

Patients should be instructed to take 20mg frusemide for each kilogram of weight gain. They will be told to do this only if they

do not have associated symptoms of dizziness.

Patients on daily diuretic therapy

If on diuretic therapy double the daily dose e.g. if on 80mg/day increase to 160mg and review weight next day. They will be told

to do this only if they do not have associated symptoms of dizziness.

Following a weight decrease of > 2 kilograms (kgs) or volume loss e.g. diarrhoea, vomiting, inability to tolerate diet and fluids.

In the event of significant weight loss of the patient will be instructed to withold their usual diuretic dose and contact their

general practitioner/HFNS to discuss the frusemide dose.

Strategies to overcome diuretic resistance include sodium and fluid

restriction, ensuring optimal pharmacotherapy (in particular ACE

inhibitors) and alteration in route and timing and combination of

diuretic agents. Intravenous therapy, including infusions, may overcome issues in bioavailability and intestinal oedema 28. 29.

D i u r e t i c d o s i n 9 in CHF In randomised trials evaluating non-diuretic treatment of heart

failure, nearly all patients with advanced heart failure (NYHA III/IV)

were treated with a loop diuretic (daily frusemide dose 80-200mg),

whereas in patients with less advanced heart failure the percentage of

patients treated with a diuretic ranged from about 20-80% ~6. These

observations reflect the importance of diuretic treatment in

management of symptomatic patients.

In most patients with advanced heart failure, a loop diuretic will be

necessary, such as frusemide (usual range 40-120mg, up to 250mg,

daily in one or two divided doses), bumetanide (1-10mg daily in

one or two divided doses), ethacrynic acid (50-100mg per day) or

torasemide, currently not available in Australia (10-50mg, up to

100rag once per day). A thiazide diuretic may be used in less severe

heart failure (e.g. hydrochlorothiazide 25rag daily). Metolazone is

a diuretic used in the United States and other settings but is not

registered in Australia.

Best practice dictates that all patients with CHF should be treated

with an ACE inhibitor (or an angiotensin ATII antagonist if ACE

intolerant) 29-33. In light of potassium sparing effects of these agents,

serum potassium levels should be monitored closely, particularly in

the context of renal impairment. The increase in prescription of

spironolactone, in community based, non-clinical trial populations,

has demonstrated a risk of hyperkalemia, not described in the

RALES trial34.

HYPONATRAEMIA AND SODIUM R E T E N T I O N IN CHF

Hyponatraemia is an independent predictor of worse survival in

patients with CHF and is indicative of advanced disease 34-42

Hyponatraemia may be attributed to diuretic treatment. More

often it is due to underlying severe heart failure leading to

stimulation of thirst, as well as non-osmotically stimulated

vasopressin release that impairs excretion of free water 30

Hyponatraemia is frequently associated with reduced diuretic

efficacy due to diminished distal tubular sodium delivery and

secondary hyperaldosteronism. Several vasopressin antagonists are

currently under clinical trial evaluation.

Altered sodium reabsorption occurs in the proximal nephron in

CHF even without congestive symptoms, due to effect of AII and

altered effective renal blood flow. Beneficial effects of ACE

inhibition suggest that the renin-angiotensin system may be

involved in early sodium retention 43.45 Resistance to atrial

natriuretic peptide has also been suggested to contribute to sodium

retention 16. Advising that patients restrict their intake of free

water may help in addressing hyponatraemia.

R o t i o n a l e for s o d i u m r e s t r i c t i o n in C H [ Non-compliance with prescribed sodium and fluid intake is a

major cause of apparent diuretic resistance 46. Kramer describes

that healthy subjects eating a high-sodium diet have a marked

increase in sodium absorption 6-24 hours after administration of

frusemide, which completely abolishes the natriuretic efficacy of a

single daily dose of frusemide, whether given intravenously or

orally ~6. Several studies indicate efficacy of diuretic therapy may

be considerably impaired due to unrestricted sodium intake in

patients with heart failure 40. Dietary sodium should be limited

below 100mmol/day 32. ,.

COMBINATION DIURETIC THERAPY

Blockade of sodium reabsorption at different sites in the nephron

has been proposed in response to stimulation of proximal and distal

tubular sodium reabsorption in patients with heart failure, treated

with a loop diuretic. When doses of more than 160mg of fmsemide

are required to relieve oedematous symptoms and normalise

elevated venous pressure, the addition of another diuretic at

another site of action of the nephron may be useful 46. The addition

of hydrochlorthiazide (25mg), metolazone (2.5mg), or

acetazolamide (250mg) may be effective ~' ~6 but may also lead to

exaggerated natiuresis and thereby aggravate renal dysfunction, so

this form of treatment mandates constant patient review.

Potassium supplementation is rarely required for individuals on

ACE inhibitor therapy and/or spironolactone.

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Aus t ra l ian Cri t ical Care

Using multiple (oral or intravenous) doses of a short-acting loop

diuretic may also minimise post-diuretic sodium rebound 4vs2.

However, it should be noted that neither of these therapies have

been subjected to randomised controlled trial evaluation.

Asymmetric dosing with a larger dose early in the morning and a

smaller dose at lunchtime may be useful. Multiple dosing strategies

may make it harder for patients to adhere with administration

advice. If medicines need to be taken in a non-hospital

environment, patients need to be involved in decision making

about the dosage schedule. Strategies such as providing a strong

rationale for the regimen, tailoring the regimen to fit in with the

person's lifestyle and use of reminders have all been shown to

facilitate 'correct' medicine taking in other settings 53.

I n d i c a t i o n s for m o d i f i c a t i o n o f d iure t i c r e g i m e n s a n d i n t r a v e n o u s d iure t i c s Demonstrable evidence of oedema indicates interstitial salt and

water accumulation when there is resistance to oral therapy.

Further, frusemide is subject to variable bioavailability 17. 2~

(Bioavailability refers to the percentage of an ingested drug that is

actually absorbed into the bloodstream). In a small sample of

healthy subjects, McCrindle and co-workers demonstrated that the

bioavailability of frusemide was markedly reduced by breakfast s4.

Intravenous administration of a loop diuretic may overcome

problems of intestinal absorption. A continuous intravenous

infusion of frusemide appears to achieve greater diuresis and

natriuresis than intermittent intravenous doses ~0 2~.47. Continuous

infusion prevents a rebound in post-diuretic sodium reabsorption,

thereby maximising diuretic efficacy. Further, frusemide

administered as an infusion causes less ototoxic effects than bolus

injections 4~.

H a e m o d y n a m i c e f fec t s a n d s u r v i v a l b e n e f i t s o f i n t r a v e n o u s l o o p d iure t i c s Intravenous loop diuretics modulate haemodynamics by reducing

wedge pressure and increasing venous capacitance, before

demonstrable evidence of diuresis 20. Improvement in

haemodynamics may be sustained during chronic treatment 17.

Sharpe and co-workers randomly assigned 60 patients with Q-wave

infarction and asymptomatic left ventricular dysfunction (ejection

fraction <45 %) to treatment with frusemide ( 40mg daily), captopril

(75rag daily), or placebo for 12 months. In both the frusemide and

placebo groups, left ventricular volumes increased and ejection

fraction decreased slightly, whereas during captopril treatment end-

systolic volume decreased and ejection fraction increased. This

study clearly demonstrates the importance of avoiding diuretic

therapy as monotherapy in CHF ss. A multi-faceted approach is

needed to target the pathophysiological process of CHF as reflected

in evidence-based guidelines 29-32.56. 57.

D o s i n g o f i n t r a v e n o u s d iure t i c s a n d a d m i n i s t r a t i o n of i n t r a v e n o u s f r u s e m i d e in the h o m e se t t ing The oral bioavailability of frusemide is 50%, so approximately

20mg frusemide intravenously is equivalent to 40mg administered

Critical Care demands technology that can remove the barriers of t ime and distance.

> transport

63 Volume 16 Number2 May2003

Aus t ra l ian Cri t ical Care

orally. Intravenous frusemide should be given 20-40mg every 1-2

hours until the desired diuretic effect is achieved, increasing the

dose by 20mg if necessary. It is recommended that IV doses be

given no faster than 4mg/minute 2~.

Intravenous frusemide can be given in the home setting by HFNS.

This action is indicated in the response to increase in oedematous

symptoms not responsive to oral therapy and/or in an emergency

situation. There is scope for this practice to occur co[laboratively

in the home setting, particularly for patients in the palliative phase

of the illness trajectory. General practitioners, HFNS and

cardiologists can work together to ensure care is performed in

accordance with the patient's wishes. Many patients wish to avoid

hospitalisation but can be admitted on a day only basis for diuretic

infusions.

Occupational health and safety issues relating to universal

precautions and safe disposal of injecting materials apply to the

home as well as hospital. Best practices of checking of medication,

aseptic venepuncture and cannulation also need to be observed.

Bolus injections can be given in the home setting, depending on

the availability of outpatient heart failure services and the goals of

therapy. Patients suitable for this technique are generally in a

symptom management phase of their illness and have had

reversible causes of oedema excluded < 2~. Administration of

infusions are problematic due to issues related to venous access and

monitoring. Management goals for patients with CHF should be to

avoid a state of crisis. Optimal medical management, adherence to

non-pharmacological strategies such as sodium restriction and

flexible diuretic regimens are important in preventing

exacerbations and crisis situations 26. 34

Eff icacy o f ACE i n h i b i t i o n The evidence that ACE inhibitor therapy improves symptoms and

mortality is indisputable 33-60. Underlying mechanisms for beneficial

effects of ACE inhibi t ion include improvement of cardiac

performance, suppression of All-mediated stimulation of thirst,

vasopressin release, and tubular sodium reabsorption. However,

administration of an ACE inhibitor, without a concomitant loop

diuretic, does not result in weight loss, natriuresis or correction of

hyponatraemia in patients with congestive signs and symptoms ~.

As previously described, the impact of diuretics on survival has not

been evaluated independently in patients with CHE The ethical

considerations in performing such a trial are considerable in

patients with symptomatic CHE Therefore, in patients with

symptomatic CHE ACE inhibitor therapy should be combined

with diuretic treatment.

N o n - s t e r o i d a l a n t i - i n f l a m m a t o r y drugs Non-steroidal anti-inflammatory drugs (NSAIDs) may contribute

to diuretic resistance by impairing renal function and the ability of

the kidney to excrete salt. These drugs may also precipitate

hyperkalaemia and acute renal failure, especially when combined

with ACE inhibitors or potassium-sparing diuretics ~

Cyclooxygenase-2 (COX-2) inhibitors block inflammatory

responses and prevent prostaglandin synthesis. COX-2 selective

NSAIDs, for example, celobrex and rofecoxib, have a similar

cardiovascular adverse effect profile as NSAIDs. Thus,

considerations related to monitoring of renal function and

electrolytes apply 62. ~. Incorporation of community pharmacists in

the patient's treatment plan can facilitate the screening of over the

counter and prescription medications.

Osteoarthritis, a common comorbidity in the elderly, is often

troublesome to patients and makes them tempted to use medication

to relieve symptoms64'% It is important to avoid them particularly

in advanced CHF and in the context of polypharmacy 66. Patients

should be encouraged to consider paracetamol as the first line of

drug therapy because of its efficacy and safety profile ~6.

THE ROLE OF HFNS IN DIURETIC MANAGEMENT

Evidence supports the role of multidisciplinary teams in CHF

management 4' 6L An important part of the nurses' role is to assist

patients in self-care strategies to facilitate disease management6S'6L

It is apparent many patients do not always follow their treatment

regimens in the way that clinicians recommend 7°73. Moreover, it is

difficult for a clinician to detect non-adherence. Perhaps the most

common method that has been employed is clinical judgement

based on 'knowing the patient'. However, several studies have

shown that clinicians are unable to detect which of their patients

are non-compliant, indicating the need for clinicians to rely on

more than clinical judgement when assessing potential adherence

amongst their patients 73.

The simplest way to detect non-adherence is to ask the patient.

Although only about one-third of patients admit non-adherence on

direct interview, those who do are to be believed. In order to

maximise the sensitivity of this approach, especially as patients are

usually reluctant to admit to non-adherence, the admission must be

socially acceptable. One study has found that health care

professionals who create a non-threatening atmosphere and who

use strategies such as open-ended questioning to gain more

information from patients, are more likely to accurately classify

people as adherent or non-adherent >.

Poor adherence amongst patients may result from inadequate

knowledge and understanding of prescribed treatment. Knowledge

of howto take the regimen is necessary before the regimen can be

followed correctly. Since patients are frequently given a great deal

of information under conditions in which they may feel tense or

anxious, it is hardly surprising that they do not remember what they

are told. In one study it was found that immediately after the visit

to the doctor, patients had forgotten two thirds of the diagnoses and

treatment explanations and one half of instructional statements 74.

In a series of studies, Ley investigated whether certain strategies

(Table 2) increased people's recall of information v3. A number of

specific techniques have been used to enhance patients' recall and

knowledge of advice. These include presenting the most important

information first, as people tend to remember this advice better.

Giving simple concrete advice, and repeating it, also enhances

recall. Explicit categorising of information, for example, dividing

the instructions into categories and announcing the categories

before giving the patient information pertaining to each category,

is another strategy to help ensure people remember information 74.

Volume16 Number2 May2003 64

Australian Critical Care

Table 2. Effectiveness of strategies for increasing recall 75.

~trategy Increase in recall Level of evidenc~

Pr imacy 3 6 % Ill

S t ress impor tance 15% III

Simplification 13% III

Expl ici t ca tegor i sa t ion 9 - 1 8 % I1-111

Repetition 14 -19% III

Specific advice 3 5 % III

Adherence with the complex regimens associated with CHF

represent a particular challenge. For example, daily weight and

observation of discernible oedema should become the key to

management of fluid status for CHF patients. This strategy is akin

to the glucometer reading for diabetic patient and the peak flow

reading for the asthmatic. Patients need to weigh themselves daily

at the same time, in similar clothing, and be encouraged to consider

an 'ideal dry weight' as occurs in renal dialysis. One way ro assist

patients remember to do this is to link the weighing to a particular

activity that takes place at the same time everyday, e.g. going to the

toilet in the morning. Digital or talking scales can be advantageous

for the visually impaired and chair scales used in nursing home and

hostel settings. Innovative methods using telecommunication

strategies are currently under evaluation to allow transmission of

vital signs and clinical data from the individual's home to a clinic

setting 7,,.

Where risk of falling is a consideration, weighing less regularly by a

family member or a health professional is a safer compromise

position. Patients and their carers should be instructed to contact

a health professional if they have diarrhoea and vomiting or

symptoms of hypotension. In summer, diuretic doses may need to

be decreased to avoid over-diuresis and hypovolaemia due to

increased insensible losses.

Patients may need assistance in timing of diuretics. Individuals

often omit diuretics for social reasons. Further, the prevalence of

urinary dysfunction and incontinence in the elderly increases the

likelihood that individuals will omit diuretics to avoid embarrassing

situations 77. Additionally, patients should also be instructed to take

their diuretics before early afternoon to avoid nocturia. In

situations where it is necessary to increase patient's diuretic dose

considerably, it is advisable to tell them to have a quiet day and not

engage in strenuous activity. This avoids potential adverse effects

of hypotension and overcomes possible increase in weakness and

fatigue.

It is important for the HFNS to understand the person's own beliefs

about their illness and treatment. The Health Belief Model

suggests that the likelihood of a person following advice is a

function of people's perceptions of the severity of the condition,

their susceptibility to its consequences and an appraisal of the

benefits and costs of following recommendations. It is the person's

subjective interpretation (i.e. what the person believes), rather

than objective reality (i.e. what the clinician knows) that is

important here 7s. To be able to help patients manage their care,

HFNS need to be aware of people's perceptions and self-

exemptions. Nurses are in an ideal position to be able to talk with

patients and elicit their relevant beliefs. Appropriate information,

such as the duration and onset of action, can then be given to help

patients to counter inappropriate beliefs.

Patients need to be assisted in strategies for management of fluid

restrictions. National Heart Foundation Guidelines recommend

1.5 litres per day and 1 litre in severe cases of CHF29. Some

negotiation with patients may be necessary, so that they feel that

they have some control over the management of their illness, for

example these restrictions may be liberalised in periods of hotter

weather. Table 3 describes strategies that may be implemented to

achieve behavioural change. Patients require tangible examples of

volume amounts and in particular need to be aware of hidden

sources of sodium such as in processed foods and to count fluid

volumes in soups, fruits and desserts. It is also important to draw

their attention to many salt substitutes that substitute potassium for

sodium as this may contribute to hyperkalaemia. In severe CHF, or

in instances of significant cognitive impairment, specific

instructions, incorporation of caregivers in the treatment plan and

practical assistance are often required.

Nur s i ng a s s e s s m e n t for d iuret ic t i t r a t i o n Nursing assessment in CHF is a complex, muhi-faceted task,

incorporating physical, social and psychological assessment (Figure

3). Physical assessment should incorporate an empirical assessment

of oedema {considering the potential for sacral oedema), evaluation

of blood pressure, heart rate, jugular venous pressure, breath sounds

and tissue perfusion. In the event of deterioration, precipitants

such as urinary tract infections should be considered. Medications

need to be noted together with biological and haematological

parameters.

The patient's ability to take responsibility for medication and self-

care regimen should be assessed. If there is suspicion of cognitive

dysfunction the use of a Mini-Mental State Examination (MMSE)

is often useful in confirming or rejecting this suspicion '~°. Riegel ~

and Jaarsma 82 have both developed and evaluated psychometric

measure to assist in determining the individual's ability to self-care.

Compliance aids such as dosette boxes, Webster Packs, diaries and

other prompts and reminders can be useful in simplifying an often

complex medication schedule 6.

Table 3. Behavioural change strategies.

Behavioural change strategies should incorporate:

• Provision of clear, specific advice

• Provision of a strong rationale

• C lea r definition of the target behav iou rs

• Opportunities for individual feedback

• Use of prompts and reminders e.g. fridge magnets and diaries

• Monitoring mechanisms via telephone, home visit or outpatient visit

65 Volume16 Number2 May2003

Australian Critical Care

Figure 3. Nursing assessment for diuretic titration.

Physical assessment • Vital signs

• Assessment for postural hypotension

• Tissue perfusion

• Jugular venous pressure

• Dependent oedema

• Breath sounds

• Assessment of NYHA 79 class

• Assessment of potential myocardial ischaemia

• Risk assessment for fall ing and sel f-care

Psychological/spiritual assessment

• Level of anxiety • Cognitive assessment

• Coping abilities • Inf luence of psychological state on

ability to self care • Level of understanding of clinical status

• Signs of depress ion and frustration • Concerns regarding condition and prognosis

Patient

assessment

Social assessment • Home situation

• Level of suppor t

• Coping ability of carer

Level of social suppor t

• Level of pr imary care support • Safety of home envi ronment

• Level of social services

• Medicat ion and t reatment plan compl iance

Clinical condition • Ascertain basel ine status

• Comorb id condit ions

• Haematological and biochemical status

• Assess whether optimally medicated

• Assess pattern of i l lness trajectory, i.e. is there a

steady deter iorat ion or sudden change

• Consider potential precipitants of clinical

deter iorat ion e.g. ur inary tract infection

• Are all key clinicians involved in the t reatment

plan aware of clinical condit ion and p lans

S e l f - c a r e d e m a , d s ~

Coping with CHF has a major impact on self-care demands. Stull

and co-workers identify that there are distinct phases in becoming

a patient with heart failure sL These include acceptance and

adjustment to the crisis event and diagnosis and the decision to get

on with life. In order to promote self-care, information is required

within a supportive-educative framework, consistent with the

individual's stage of adjustment, ability to self-care and

incorporating family members and significant others 6. 2~. 7s. 8~

Information and education plans should:

• Incorporate the individual and significant others.

• Individualise strategies for changing health behaviours (Table 3).

• Encompass a clear and unambiguous treatment plan.

• Foster initiative and independence.

• Ensure information is socially and culturally relevant ~.

CONCLUSIONS

It is important in the management of patients with CHF to

remember that with the exception of the RALES trial, diuretics

have not demonstrated an improvement in survival. Therefore,

diuretics should never be used as monotherapy but as adjunctive

therapy to agents with demonstrated survival benefit, such as ACE

inhibitors and beta-blockers.

The uptake of best practice guidelines with respect to optimal

medical therapy have repeatedly demonstrated disappointing

rates in 7''84'~s. This is likely attributable to the dynamic state of

CHF and the complexity of both pharmacological and non-

pharmacological t reatment regimens. It is evident from

guidelines that diuretic requirements often fluctuate with the

initiation of pharmacological agents and changes in patient's

condit ion a~.

Volume16 Number2 May2003 66

AK Australian Critical Care

HFNS are well placed to disseminate best practice guidelines and

facilitate their implementat ion 26. Titration of diuretics is often a

critical factor in achieving optimisation of therapies such as beta-

blockers. Prasun has evaluated a diuretic t i tration protocol that

allowed heart failure patients to adjust their diuretic medication

dose based on symptoms of fluid re tent ion so. Patients were

randomised into a usual care group or a patient-directed diuretic

t i tration group and followed for three months. The use of the

patient-directed diuretic protocol was associated with a significant

improvement in exercise tolerance and quality of life, fewer ED and

hospital admissions.

HFNS are also critical in providing information, support and

infrastructure to enable patients and their families to cope with the

demands of CHE This role is performed within a team work approach

in which collaboration with physicians and other health care workers

is emphasised. To competently and proficiently perform this role,

within a quality use of medicines approach, HFNS must possess a

sound knowledge of the physiology of CHF and an appreciation of the

pharmokinetics and pharmacodymamics of the agents used to treat

this condition st. Close physician and pharmacy clinical supervision is

also necessary t o support HFNS in this specialist role-Z

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heart failure. Heart 2000; 83:596-602.

2. Krum Het al. National Heart Foundation of Australia and Cardiac Society of Australia & New Zealand Chronic Heart Failure Clinical Practice Guidelines Writing Panel. Guidelines for management of patients with chronic heart failure in Australia. Medical Journal of Australia 2001 May 7;174(9):459-66.

3. Krum H, Tonkin AM, Currie R, Djundjek R & Johnson C[. Frequency, awareness and pharmacological management of chronic heart failure in Australian general practice. The Cardiac Awareness Survey and Evaluation (CASE) Study. Medical Journal of Australia 2001; 174(9):459-466.

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20. Dormans TP & Gerlag PG. Combination of high-dose frusemide and hydrochlorothiazide in the treatment of refractory congestive heart failure. European Heart Journal 1996; 17:1867-i874.

21. Micromedex. http://micromedec.hcn.net.au. Accessed 5 November, 2001.

22. Krumholz HM, Chen YT, Wang Y, Vaccarino V, Radford MJ & Horwitz RI. Predictors of readmission among elderly survivors of admission with heart failure. American Heart Journal 2000; 139:72-7.

g Calvary

Heallb C~re Tasmania

C L I N I C A L N U R S E M A N A G E R

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This is an outstanding opportunity to provide leadership in the clinical management and coordination of Critical Care Services at Calvary Health Care Tasmania.

Do you have the following skills to lead this successful and progressive Unit? Essential criteria: • Proven management, organisational and leadership skills • Sound clinical judgment and commitment to best practice • Clinical cempetance • Ability to initiate and implement quality programs • Customer focused • Excellent communication and interpersonal skills • Assistance with travel and accommodation available

Come and join the premier private hospital and enjoy the benefits of the Island state. Hobart offers you all that you expect in city life - food, wine and entertainment. Tasmania has one difference....it is a relaxed and friendly environment where in a few minutes you can escape to our pristine wilderness, beaches and heritage towns.

All enquiries to: Forward applications addressing Geoff Wieczorski above criteria to: Nursing Services Coordinator Sally Faulkner Calvary Health Care Tasmania Director of Nursing Telephone: (03) 6278 5235 Calvary Health Care Tasmania Email: q.wieczorski~calvarytas.com.au GPO Box 1523

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67 Volume 16 Number2 May2003

Australian Critical Care

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Volume16 Number2 May2003 68

Australian Critical Care

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Chest x-ray quiz

Answer and discussion

There is marked pneumopericardium (arrowed). Sternal wires are evident. The central venous line is projected over the superior vena cavae (arrowed). The endotracheal tube has been removed. There is subsegmental areas of atelectasis at the right base (arrowed).

These look like Kerley B lines, but as the lung fields do not show any evidence of pulmonary oedema, these lines are much more likely to be small areas of atelectasis. There is also a small right sided pleural effusion.

For question turn to page 45 of this issue.

69 Volume16 Number2 May2003