Heart Failure : A Case Study

INTRODUCTION
Fluid resuscitation in severely critical patients can be challenging, particularly when the patient is in cardiogenic shock with pulmonary
edema and hypoxia needing mechanical ventilation.Traditional hemodynamic monitoring parameters obtained via a pulmonary artery catheter do not address the issue of fluid responsiveness in patients on mechanical ventilation. In this case study,
we describe the use of stroke volume variation (SVV) monitoring, which guided our decision to add fluids in order to improve cardiac
output (CO). SVV guided fluid optimization led to a successful outcome in this seriously ill patient.
CLINICAL EVENTS
Patient Details: 32-year-old male
Medical History:
Diagnoses: type 2 diabetes; idiopathic dilated cardiomyopathy
with left ventricular ejection fraction (LVEF) of 20%.
Receiving optimal anti-heart failure therapy of torsemide,
ramipril, carvedilol, digoxin, plus insulin.

Heart Failure Case Study
SVV Guided Fluid Therapy in a Case of Heart Failure with Hypotension

CASE NOTES
The patient was admitted with chief complaints of progressive dyspnea even at rest (NYHA Class IV heart failure) and swelling of
feet. He was in sinus rhythm, his heart rate was 90 beats/minute,blood pressure was 108/60 mmHg, (mean arterial pressure
78 mmHg), respiratory rate was 22/minute.
He was treated with intravenous diuretics, nitroglycerin, dobutamine and mask oxygen.
The patient was evaluated and referred for cardiac resynchronization therapy (CRT).

Investigations before CRT:
- Hemogram: Hb – 11.9 gm%, total leucocyte count (TLC) –11,000/cmm, platelets – 252,000/cmm.
- Blood urea levels (BUL) – 24 mg%, serum creatinine – 1.1mg%,serum sodium – 132 mEq/L, serum potassium – 3.5 mEq/L,serum chloride – 97 mEq/L.
- Blood sugar levels were well controlled on insulin.
- ECG showed LBBB pattern with QRS duration of 146 msec.
- Chest x-ray showed cardiomegaly with bilateral lower zone haziness suggestive of pulmonary edema.
- Pre-procedure echocardiographic evaluation showed dilated cardiomyopathy with global hypokinesia, LVEF 20%,Grade I mitral  
  regurgitation  with mild pulmonary hypertension with pulmonary arterial systolic pressure (PH) of 38 mm.

CRT procedure:
The patient underwent CRT in the form of bi-ventricular pacing under general anesthesia. Drugs used during the procedure
were fentanyl 100 mcg, midazolam 4 mg, and ketamine 50 mg for induction and propofol 1-1.2 mg/min for
maintenance. Total procedure time was 5 hours. Patient required dopamine 5-8 mcg/kg/min throughout the procedure
to maintain blood pressure. Central venous pressure (CVP) and intra-arterial blood pressure monitoring was performed
throughout the procedure. Advanced hemodynamic monitoring (such as PA catheter, arterial pulse based cardiac
output, transpulmonary thermodilution methods or transesophageal echo-Doppler) was not used during the procedure.


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Ventilatory requirements during the procedure were high due to cardiogenic pulmonary edema. Patient received 60 mg of
furosemide during the procedure. Patient was ventilated with pressure- controlled ventilation, peak inspiratory pressure of 35 cm,
PEEP of 10 cm, and FiO2 of 1. Intra-operative ABG values were:
pH – 7.19, PO2 – 62 mm, PCO2 – 74 mm, HCO3 – 28.3 mmol/L.
Intra-operative blood loss was 300 ml and urine output was 1200 ml.
The patient received 500 ml of Ringer’s lactate during the procedure.

Post-CRT:
After the CRT procedure, the patient was moved to the Intensive Care Unit (ICU). Hemodynamic and ventilatory issues identified in
the ICU were:
- HR 130/min, sinus rhythm, BP was 84/50 mmHg on dopamine 14 mcg/kg/min, MAP was 61 mmHg.
- Severe hypoxia. Volume-controlled ventilation, tidal volume -500 ml, respiratory rate – 18/min, needing PEEP of 12 cm with
FiO2 of 0.7, peak inspiratory pressure reaching 41 cm with plateau pressure of 32 cm.
- CVP was persistently in the 18 to 20 mmHg range.
- 1000 ml negative fluid balance while in operating room.

At this point, our therapeutic dilemmas were:
1. If we give fluids to correct negative fluid balance, there was risk of aggravation of pulmonary edema, as the patient was already
extremely hypoxic. Secondly what would be our goal or target forfluid therapy?

2. If we escalate dopamine to achieve higher perfusion pressure, there is risk of worsening of tachycardia and further deterioration
of cardiac function, plus the risk of high-dose dopamine in terms of renal hypoperfusion and subsequent renal impairment.

3. To achieve afterload reduction and improvement in cardiogenic pulmonary edema, nitroglycerin or nitroprusside could not be
given, as the BP was very low (same concern about dobutamine).

4. At such low MAP, would diuresis have an effect?
We decided to monitor cardiac output, cardiac index, systemic vascular
resistance index (SVRI) and stroke volume variation (SVV)

for better hemodynamic monitoring to get answers to these questions:

1. Is cardiac output adequate?
2. What is peripheral vascular resistance?
3. Is this shock fluid-responsive?
A radial arterial line was connected to the FloTrac system and hemodynamic variables displayed on the Vigileo monitor (see
table). There were no arrhythmias. The patient was under deep sedation and paralysis on controlled mechanical ventilation. We
obtained repeated SVV values by making Vt 8 ml/kg. SVV was between 20% and 22%.

Hemodynamic monitoring values:
CO 4.7 l/min
CI 2.6 l/min/m2
SVV 20%
SVRI 1261

We felt that this information offered significant and fairly reliable evidence of preload dependency of this hemodynamic insufficiency.
Therefore, we administered the first fluid bolus of 250 ml of 0.9% isotonic NaCl in 30 minutes, which resulted in marginal improvement
in CO to 5 l/min, and MAP increased to 66 mm.

Fluid boluses were continued until SVV dropped to < 15% on controlled ventilation. A total of 2450 ml fluids were given in the 14
hours post-operatively. MAP improved with fluid boluses and dopamine was rapidly tapered to 5 mcg/kg/min at the end of 6
hours in the ICU. HR settled to 100/min. Dobutamine was started at 5 mcg/kg/min to improve cardiac output and nitroglycerin was
administered. Once hemodynamic stability was achieved, 40 mg of furosemide was given.

The patient’s ventilatory requirements reduced rapidly and he was extubated 24 hours after ICU admission. Dobutamine was continued
for the next 24 hours and tapered gradually. Ramipril and digoxin were restarted. BSLs were controlled with insulin infusion.
Five days post-procedure, cardiac evaluation via 2D echocardiography and Doppler showed improved LV function to 25%, and PH
was marginally reduced. The patient was discharged from the hospital on day 7.

DISCUSSION
We feel that CO, CI and SVV monitoring helped us immensely in improving this patient’s critical hemodynamic condition. If we had
monitored only MAP, CVP or PAOP in this kind of acute cardiogenic pulmonary edema plus cardiogenic shock, fluid resuscitation
would not have been attempted, and the outcome would likely have been far less successful. Instead, with the indication that the patient
would respond positively, we could proceed confidently with fluid replacement. Further, the SVV parameter guided us regarding
when to stop administering fluids.

CaseStudy:Heart Failure

 

Case Study Results

Results in summary

One thousand four hundred andtwenty eight responses have been received to thiscase study and the aggregateresults of one hundred responses have been compiled for

feedback.

All respondents identified riskfactors for heart failure and gave lifestyle advice forthe management of the condition.Most respondents specified at least one of the therapeutic goals of ACEinhibitor therapy.84% of respondents used startingdoses of ACE inhibitor therapy which were low doses and these were inaccordance with those recommended in Therapeutic

Guidelines: Cardiovascular 3rd edition.1 The mostcommonly prescribed ACE inhibitors were perindopril 2mgdaily (38%)* and lisinopril 2.5mg daily (12%)*.90% of respondents prescribedtarget maintenance doses, which have demonstrated mortality benefits.1 Most commonlyprescribed maintenance therapy were perindopril 4-8mg daily (39%)* and lisinopril20-40mg daily (17%)*.

Most respondents chose tocontinue frusemide as an adjunct to ACE inhibitor therapy (86%)*. Frusemide 40mg daily wasthe most common choice (55%)* while 36% chose low dose frusemide 20-40mgdaily.

Regular monitoring of bloodpressure, signs of peripheral oedema, urea & electrolytes and serum creatinine / renalfunction were most commonly instituted by the respondents.81% of the respondents identifiedthe need to cease or minimise use of diclofenac (a NSAID) in a patient with heartfailure.

Results in detail

Question 1

What lifestyle advicewould you give Mr James?

95% of respondents would discuss3 or more non-pharmaceutical measures with Mr

James. These responses are listedbelow.

Lifestyle AdvicePercentage of

Respondents *

Sodium restriction 87

Exercise: moderate, regular or graded81

Weight reduction and/or low fat diet79

Fluid restriction to 1.5 litres perday 67

Cessation of smoking 40

Cessation /reduction of alcohol intake25

Monitoring daily weight 12

Monitoring blood pressure, diabetes,cholesterol levels 11

Nutritional advice 4

A structured educational program 2

Other 4

* Respondents may have indicatedmore that one response

Question 2

What is thetherapeutic goal of the ACE inhibitor therapy?

96% of respondents were able toidentify one or more goals of ACE inhibitor therapy.

These responses are summarized inthe table below.

Goals of ACEinhibitor Percentage of

Respondents *

To improve prognosis 35

To reduce symptoms /to reducemorbidity 35

To reduce the rate of hospitalistion31

To improve exercise tolerance 32

To improve quality of life 27

To reduce mortality 25

To improve cardiac function /LVF 20

To aim for highest tolerated dose 15

To reduce afterload on myocardium 7

Other 5

* Respondents may have indicatedmore that one response

5

Question 3

What would you prescribe as initial ACE inhibitor therapy?

84% of respondents initiatedstarting doses of ACE inhibitor, which corresponded to those outlined in the TherapeuticGuidelines: Cardiovascular 3rd edition.1 The responses are shown in the tablebelow.

ACE inhibitor Brand name Recommended starting dose 1 Respondent choices of starting doses

Perindopril Coversyl 2mg daily 2mgdaily

2-4mg daily

Lisinopril Prinivil, Zestril 2.5mgdaily 2.5mg daily

5mg daily

30mg daily **

Ramipril Ramace, Tritace

1.25mg daily 1.25mg daily

1.25-2.5mg daily

2.5mg daily

616 Enalapril Amprace, Renitec

2.5mg daily 2.5mg daily

2.5 mg BD

5mg daily

Captopril Acenorm, Capace,Capoten, Captohexal, DBL, Enzace, SBPA

6.25mg BD 6.25mg BD

12.5mg BD

Fosinopril Monopril 5mg daily 5mgdaily 5

Quinapril Accupril, Asig 2.5mg daily2.5mg daily

Trandolapril Gopten, Odrik 0.5mg daily0.5mg daily 2

Question 4

What would be your target maintenance dose of ACE inhibitor?

90% of respondents prescribed target maintenance doses, which corresponded to those outlined in the Therapeutic Guidelines: Cardiovascular 3rd edition.1 The responses are shown in the table below.

ACE inhibitor Brand name Recommended target maintenance dose 1 Respondent choices of targetmaintenance dose

Perindopril** Coversyl 4-8mg daily 2mgdaily

Lisinopril Prinivil, Zestril 20-40mgdaily 20-40mg daily

Ramipril Ramace,Tritace

Enalapril Amprace,Renitec

Captopril Acenorm,Capace,Capoten,Captohexal,DBL, Enzace,SBPA

Fosinopril Monopril 20-40mg daily 20mgdaily

Quinapril Accupril, Asig 20-40mg daily5mg daily

Question 5

Would you continuethe frusemide?

86% of respondents chose tocontinue the frusemide as an adjunct to ACE inhibitor

therapy. 12% elected not tocontinue it and 2% did not specify. Of the 12% that

choose not to continue frusemide,9% offered a reason. Examples of such included

waiting to see if the ACEinhibitor controlled symptoms and waiting until the target

dose was reached. If it wasrequired, 2 respondents chose low dose frusemide while 2

other respondents choseindapamide.

Question 6

If so, at what dose?

55% of respondents chose tocontinue frusemide 40mg daily and 36% chose low dose

frusemide 20-40mg. 97% ofrespondents chose a frequency of daily for the frusemide.

The total daily doses chosen areshown in the table below.

Total daily dose offrusemide (mg) Percentage of

Respondents

40mg 55

20-40mg 20

20mg 16

40-80mg 7

80mg 3

40-120mg 1

Question 7

What monitoring wouldyou institute?

All respondents would monitor oneor more clinical signs.

Clinical signs Percentage of Respondents *

Blood pressure /hypotension 69

Ankle oedema /oedema /peripheraloedema 59

Bibasal creps /lung crepitations/breath sounds /crackles

/pleural effusion

52

Weight 48

Jugular venous pressure 39

Pulse-rate, rhythm 26

Degree of dyspnoea /SOB /orthopnea/paroxysmal nocturnal

dyspnoea/cough

24

Heart sounds /triple rhythm /S3 13

Exercise capacity 7

Cardiomegaly 6

Hepatomegaly /splenomegaly 5

Signs of heart failure (unspecified) 5

Other 1

* Respondents may have made more thanone response.

8

97% of respondents wouldinvestigate biochemistry.

BiochemistryPercentage of

Respondents *

Urea & electrolytes 98

Creatinine /renal function 74

Full blood count (including Hb) 12

Liver function tests 7

Lipid profile 7

Blood sugar levels 6

Erythrocyte sedimentation rate /CRP 2

Urinary microalbumin 2

Thyroid function tests 1

Urine analysis 1

Unspecified 3

*Respondents may have made more thanone response

Question 8

What medicationcounselling would you give to the patient?

99% of respondents would providemedication counselling. 81% of respondents

would cease or minimisediclofenac (a NSAID) and of these most would offer regular

paracetamol as an alternative. Asummary of responses is shown below.

MedicationCounselling Percentage of

Respondents *

Cease or minimise diclofenac (a NSAID)81

Explain need for regular, indefiniteACE inhibitor /diuretic

therapy

36

Explain side-effects of drugs &instruct to report if occur 27

Suggested regular physical examination& biochemistry 14

Report concurrent use of othermedication including OTC 4

Report if cough develops 4

Watch for first dose hypotension 4

Suggested non-pharmacological treatmentsof OA 3

Explain potential changes tomedication & dosages 3

Avoid potassium supplements 2

Take asprin regularly 1

Do not alter medications 1

Prescribed Fluvac® & Pneumovax® 1

*Respondents may have made more thanone response

9

Expert commentary

Associate ProfessorPeter MacDonald

Staff Cardiologist,St Vincent’s Hospital, Sydney.

The case history presents bothdiagnostic and therapeutic issues. Only the therapeutic issues have been addressed indetail by the questions posed about this case.The diagnosis of heart failuredue to systolic left ventricular dysfunction is clear enough from the informationprovided, however the underlying pathological process that has caused the LVdysfunction has not been determined. The most likely cause in our community is ischaemic heartdisease, but long-standing hypertension or some form of dilated cardiomyopathyare also possibilities. A history of angina, myocardial infarction, hypertension, othercoronary risk factors should be sought and alcohol consumption assessed.

The overall case study resultsindicate that the vast majority of GPs have a clear understanding of the importanceof life-style modifications and the appropriate use of ACE inhibitors in patients withheart failure. The importance of non-steroidal antiinflammatory

drugs as a precipitant of heartfailure has been recognised as has the importance of regular monitoringof blood pressure and signs of fluid retention, and simple blood tests to measureelectrolytes and creatinine. The optimal use of ACE inhibitors, diuretics andbeta-blockers in patients with heart failure is critically dependent on this type ofmonitoring.

Question 1

What lifestyle advicewould you give Mr James?

I would emphasize the importanceof salt restriction and encourage regular lowintensity exercise. His abilityto exercise may be limited by his osteoarthritis and it would be necessary to establishhis limitations due to OA before embarking on a course of exercise. Aphysiotherapist should be able to provide an appropriately structured exercise program whichtakes into account restrictions caused by other disabilities. Fluid restrictionin addition to salt restriction is usually only required in patients with intractable oedema.The patient should be screened for all coronary risk factors and advised to stopsmoking if this is the case. Alcohol should be minimised or stopped completely if analcoholic cardiomyopathy is considered likely.

Question 2

What is thetherapeutic goal of the ACE inhibitor therapy?

The goals of ACE inhibitortherapy are multiple and vary according to the individual. For example, prolongation of lifeis clearly a major goal in this 68 year old man, but may not be if he were 88 yearsold. Improvement in quality of life and prevention of the need for hospitalisation areimportant goals of ACE inhibitors in all patients.Improvements in exercisetolerance and cardiac function are usually modest, but are important in as much as theycontribute to the patients improved quality of life and symptomatic stability.

Question 3

What would youprescribe as initial ACE inhibitor therapy?

The patient should be started onan ACE inhibitor in low dose. Although the benefits of ACE inhibitors are almostcertainly a class effect, my preference is to choose a once daily ACE inhibitor in orderto facilitate compliance.

Question 4

What would be yourtarget maintenance dose of ACE inhibitor?

The target dose of ACE inhibitorshould be that which has been shown to be effective in clinical trials. The majorityof respondents have answered this question appropriately. Surveys ofprescriptions written for heart failure drugs suggest,however, that most ACE inhibitorsare prescribed in low doses.

Question 5

Would you continuethe frusemide?

I would continue to prescribefrusemide in this patient. It is tempting to think that use of a single agent such as an ACEinhibitor may be sufficient to control a patient’s symptoms. Most patients withsymptoms and signs of fluid retention do require a diuretic to achieve optimalsymptomatic control.

Question 6

If so, at what dose?

It may be possible to reduce thedose of frusemide, but as stated above in response to Question 5, it is unlikely thatthe patient will remain asymptomatic on an ACE inhibitor alone. Concurrentdiuretic administration renders patients more prone to symptomatic hypotension after theintroduction of an ACE inhibitor. It would be important to check the patientsblood pressure, serum sodium and creatinine prior to

commencement of an ACE inhibitor.If the blood pressure or serum sodium is low, orthe serum creatinine is elevated,I would halve frusemide dose at the time of commencement of the ACEinhibitor.

Question 7

What monitoring wouldyou institute?

Clinical and laboratory parametersare both important in judging the response to heart failure therapy. Blood pressureis obviously important in determining the use and dose of ACE inhibitor. Caution isrequired in patients with a systolic BP<100mmHg and any patient with a systolicBP<90mmHg prior to introduction of an ACE inhibitor should be referred to aspecialist. Symptoms and signs of fluid retention are important in determining the doseof diuretics and the use of beta-blockers. Betablockers should only be administered topatients who have been rendered ‘euvolaemic’.Regular monitoring ofelectrolytes and renal function is important in patients receiving diuretics and ACEinhibitors, particularly during changes in therapy.Measurement of serum lipids,glucose, haemoglobin and thyroid function tests are important in the initialdiagnostic evaluation, but need not be repeated on a regular basis unless abnormal or newsymptoms develop.

Question 8

What medicationcounselling would you give to the patient?

The importance of NSAIDs as aprecipitant of heart failure has been identified by the majority of GPs and I wouldcertainly advise the patient to stop this medication.COX-2 inhibitors have noadvantages in this patient and paracetamol is probably the safest alternative. I believethat some time is needed to explain the rationale for the use of an ACE inhibitor, possibleside-effects including first dose hypotension (and how the risk of this may beminimised eg by taking the first dose at night before bed) and cough, and the need tocontinue this treatment permanently. The importance of regular medical follow-up alsoneeds to be emphasized.

Dr Mark Morris

General Practitioner,Spring Hill, Queensland

Mr James sounds all too familiar;a male patient presenting in his sixties or older with a history of increasing shortnessof breath on exertion. There is often a history of smoking and hypertension but weare not given this information. The most likely causes of his heart failure areischaemic heart disease and hypertension and both conditions may be present. Thisis based on the fact that 90% of all cases of heart failure are due to hypertensionand ischaemic heart disease. There may be a few clinical signs of heart failureand I would stress the importance of moving on to an echocardiogram early to prove ordisprove the diagnosis and assess the severity and cause.

Question 1

What lifestyle advicewould you give Mr James?

In the hurry to get a patient onmedication, lifestyle advice can easily be forgotten and I was pleased to see in theresponses to question 1 that 95% of respondents would discuss 3 or morenon-pharmaceutical measures with Mr James. The important interventions were all mentioned:smoking cessation, alcohol reduction or cessation,weight reduction if overweight,sodium restriction, moderate regular exercise when heart failure stable, fluidrestriction in patients with hyponatraemia and monitoring weight.

Question 2

What is thetherapeutic goal of the ACE inhibitor therapy?

ACE inhibitors should beprescribed in all patients with heart failure, unless there is a specific contraindication. ACEinhibitors improve prognosis, reduce hospital admissions and improve quality oflife and the answers to the questions on ACE inhibitors indicate that therespondents are aware of the benefits.

Question 3

What would youprescribe as initial ACE inhibitor therapy?

Question 4

What would be yourtarget maintenance dose of ACE inhibitor?

The importance of starting at alow dose and titrating up is understood but I would like to stress the importance oftitrating to the maximum dose over 3 to 4 weeks. If the patients becomes hypotensivewhile titrating up then the appropriate response is usually to reduce the diureticand not the ACE inhibitor. Remember to monitor renal function and electrolytes andthat careful dosage titration and closer monitoring is required in the elderly.Generally, ACE inhibitors still tend to be under used and prescribed in suboptimal doses.

Question 5

Would you continuethe frusemide?

Question 6

If so, at what dose?

Like the majority of respondents,I would continue frusemide as an adjunct to the ACE inhibitor therapy. Thefrusemide would contribute to the control of the signs and symptoms of heart failure.The dose of frusemide may need to be reduced to 20mg daily as the dose of ACEinhibitor is increased.

Question 7

What monitoring wouldyou institute?

Monitoring heart failure patientsmust include checking renal function, electrolytes and blood pressure, and this wasidentified by the majority of respondents. In addition to this, patients shouldbe regularly assessed for signs and symptoms of heart failure and have other pathologychecks periodically or when indicated e.g. full blood count, liver function tests,blood glucose, lipids and thyroid function tests. Asking patients to check their weightdaily provides an extra guide on clinical status and treatment response.

Question 8

What medicationcounselling would you give to the patient?

The message has been around foryears and is obviously well known that NSAIDs can exacerbate heart failure. I agreewith the majority of respondents that diclofenac should be stopped if possible andI would try using regular paracetamol and nonpharmacological measures to control his symptomsof osteoarthritis. Unfortunately, the new selective COX-2inhibitors appear to cause the same problems in heart failure as the older NSAIDs. Respondentsalso identified the important issue of encouraging compliance with antifailuretherapy, including reporting side effects. Reminding patients to discussover-the-counter and complementary medications before taking them is important.Over-the-counter NSAIDs and potassium supplements are not uncommon discoveries when asking heartfailure patients about other tablets, vitamins, tonics or supplementsthat they take. Vaccination annually with the influenza vaccine and 5 yearlywith Pneumovax®wasmentioned and should be given.Treatment of heart failure andunderlying disease(s) and risk factors does involve an increasing number of medications.In this case, Mr James would also be considered for a beta-blocker e.g.carvedilol, and he may also require lipid lowering medication and other medication. Compliancecould be a significant issue and it is obviously important to involve Mr James indecisions about his treatment and continue to check compliance. Promptly addressside-effects and reinforce the benefits of treatment at follow-up visits.

Reference

1. Therapeutic Guidelines: Cardiovascular,3rd edition. North Melbourne:

Therapeutic Guidelines Limited, 1999:111-125