ahfailure-170609065615-converted.pptx

TEXT
ACUTE DECOMPENSATED HEART FAILURE
▸Ingo Moeller
▸SCGH Registrar Teaching 08/06/2017

CLINICAL VIGNETTE - MY PATIENT FROM
SATURDAY NIGHT
Its 6:32 am and you are the Registrar in charge of the Saturday night shift at Charlie’s.
You are tired after battling through Amphetamine and ETOH inebriated Patients, its quiet,
….too quiet!
“Its quite quiet” the Intern says…… and 2 minutes later SJA rushes a patient into T2.
The patient is an overweight middle-aged man who is also struggling
to breathe. SJA report that his blood pressure was 220/130 mm Hg at the scene.
Shifty immediately attaches the patient to the cardiac monitor and obtains vital signs.
His blood pressure is now 240/140 mm Hg. HR is 140. You listen to his lungs and notice coarse, wet breath
sounds. Your patient is tachypnoeic, sweaty, leaning forward in bed, and saturating 72% on room air. His oxygen
saturation improves to 88% on a 100% nonrebreather mask.
His legs are oedematous, and he has marked conversational dyspnea(single words).
Respiratory arrest seems certain unless appropriate action is taken, and you wonder what to do…..

ACUTE HEART FAILURE
INTRODUCTION…..
▸incidence of in-hospital mortality among patients admitted to the hospital
for decompensated heart failure is 6.4%
▸in individuals aged 65 to 69 years, the prevalence of heart failure is
roughly 20 per 1000,
▸Among people >65 years of age presenting to primary care with
breathlessness on exertion, one in six will have unrecognized HF
(mainly HFpEF)
▸prevalence jumps to more than 80 per 1000 in individuals older than 85
years.

ACUTE HEART FAILURE
▸Acute heart failure (AHF) is a relevant public health problem
causing the majority of unplanned hospital admissions in
patients aged of 65 years or more.
▸AHF was historically described as a pump failure with
downstream hypoperfusion and upstream congestion.
▸AHF remain poor with 90-day rehospitalization and 1-year
mortality rates reaching 30%
Understanding acute heart failure: pathophysiology and diagnosis, Eur Heart J Suppl (2016)

EPIDEMIOLOGY OF HEART
MORE DEATHS FROM
HEART FAILURE THAN
FROM ALL FORMS OF
CANCER COMBINED
550,000 NEW CASES/YEAR
4.7 MILLION SYMPTOMATIC
PATIENTS;
ESTIMATED 10 MILLION IN
2037
*Rich M. J Am Geriatric Soc. 1997;45:968–974.
American Heart Association. 2001 Heart and Stroke
Statistical Update. 2000.
3.5
4.7
10
0
2
4
6
8
10
F
12 AILURE (IN THE US)
1991 2000 2037*
Heart
Failure
Patients
in
US
(Millions)

NOT ALL HEART FAILURE IS THE
SAME.
- Heart failure with preserved ejection fraction (HFpEF)
- and heart failure with reduced ejection fraction (HFrEF)
- may present with either hypertension or hypotension
-represent distinct underlying pathophysiologies that
require different approaches in treatment.
-HFpEF and HFrEF are equal in terms of occurrence,
morbidity, and mortality.
Karrowni W, Chatterjee K. Diastolic heart failure: the current understanding and approach for management with focus on intensive care unit patients. J Intensive Care Med. 2014;29(3):119-127. (Review article)

SYSTOLIC AND DIASTOLIC HEART FAILURE
Heart failure occurs when the heart is either unable-
-to Pump blood during systole (HFrEF) or
-to Fill with blood during diastole (HFpEF)
Systolic heart failure results in heart failure with reduced ejection fraction. Diastolic heart failure results in heart failure with preserved ejection fractio

HEART FAILURE WITH PRESERVED
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nfraction that is either borderline (41%-
49%) or normal (> 50%).
Diastolic dysfunction
is characterised by elevated left ventricular filling pressures with impaired myocardial
relaxation.
responds differently to traditional heart failure therapies that were intended for the
traditional treatment of HFrEF

ETIOLOGY AND PATHOPHYSIOLOGY
▸Injury to Myocardium
▸secondary to a number of causes that develop slowly over time (uncontrolled
hypertension, diabetes) or
▸more suddenly (eg, coronary ischaemia, STEMI)
▸Regardless of the cause, myocardial injury results in
▸structural-abnormalities of the ventricular wall that impair systolic
contraction or diastolic relaxation
▸electrophysiological, ->impaired conduction,(QRS widening on ECG),
which can lead to conduction blocks and re-entrant dysrhythmias and
▸biochemical remodeling -> impaired myocyte functionality and
increased risk of dysrhythmia

THE ISSUE IS…
▸Regardless of the underlying aetiology, patients presenting
with AHF appear very similar to each other:
▸Sodium and Fluid retention,
▸excess Fluid backing up into the lungs, abdomen, and
extremities.
▸The result is fatigue, peripheral oedema, and dyspnea that
is often worse with exertion

PATHOPHYSIOLOGY OF ACUTE HEART FAILURE
▸Acute heart failure is defined as new-onset or worsening of
symptoms and signs of HF
▸AHF typically includes symptoms or signs related to
congestion and volume overload rather than to
hypoperfusion
▸level of congestion and the number of congested organs
have prognostic relevance in HF patients
Gheorghiade M. European Society of Cardiology, European Society of Intensive Care
Medicine. Assessing and grading congestion in acute heart failure: a scientific statement
from the acute heart failure committee of the heart failure association of the European
Society of Cardiology and endorsed by the European Society of Intensive Care
Medicine. Eur J Heart Fail 2010

CIRCLING THE DRAIN

PATIENT EVALUATION IN ED
▸history,
▸physical examination,
▸chest radiography,
▸12-lead ECG,
▸Troponin
▸electrolytes, and a
▸complete blood cell count
▸BNP
Collins SP, . Prevalence of negative chest radiography results in the emergency department patient with decompensated heart failure. Ann Emerg Med. 2006;47:13–18.

DIFFERENTIAL DIAGNOSIS
▸look for alternative diagnoses
▸do not miss reversible causes and
▸other life threatening causes

CAUSES OF AHF

PRECIPITANTS AND DIFFERENTIAL
DIAGNOSIS
▸Differential Diagnosis for Patients
Presenting With Dyspnea
▸Life-Threatening causes
▸Decompensated heart failure
▸Chronic obstructive pulmonary
disease
▸Asthma
▸Pneumonia
▸Pulmonary embolism
▸Acute coronary syndromes
▸Aortic dissection
▸Pericarditis or pericardial effusion
▸Pneumothorax
▸Precipitants of Acute heart failure
▸Acute coronary ischaemia
▸Valvular dysfunction
▸Cardiac arrhythmia
▸Pulmonary embolism
▸Myocarditis
▸Hypertensive emergency
▸Pericardial tamponade
▸Severe anemia
▸Worsening renal failure
▸Sepsis
▸Drug noncompliance
▸Dietary indiscretion
▸Medication side effect / change
▸Thyroid dysfunction

HISTORY TAKING PEARLS ON SEVERITY OF
UNDERLYING DISEASE
▸Expect more severe disease in Patients with
▸AICD or PPM (automated implantable cardioverter defibrillator
▸Medication clues e.g. Patient on Spironolactone
▸Patients on homeopathic doses of Beta Blockers or ACE might
have baseline low BP
▸whilst patients with big doses are truely Hypertensive’s at baseline
▸Weight change if known?

AHF - SIGNS AND SYMPTOMS
▸Exertional dyspnea and/or dyspnea at rest
▸Orthopnea
▸Acute pulmonary oedema
▸Chest pain/pressure and palpitations
▸Tachycardia
▸Fatigue and weakness
▸Nocturia and oliguria
▸Anorexia, weight loss, nausea
▸Exophthalmos and/or visible pulsation of eyes
▸Distention of neck veins
▸Weak, rapid, and thready pulse
▸Rales, wheezing
▸S 3 gallop and/or pulsus alternans
▸Increased intensity of P 2 heart sound
▸Hepatojugular reflux
▸Ascites, hepatomegaly, and/or anasarca
▸Central or peripheral cyanosis, pallor
▸Big Ticket items:
▸Patient Position
▸Hypertensive/Hypotensive
▸Distention of neck veins - Surrogate
for Right Heart pressure
▸Auscultation —>Rales, wheezing -
worse rales>worse AHD
▸New Heart Murmur / Distant Heart
sound
▸S3 gallop - Diagnostic for AHD
▸uni/bilateral Leg swelling

ASSESSMENT OF HF PROBABILITY
▸1. Clinical history:
▸History of CAD (MI, revascularization)
▸History of arterial hypertension
▸Exposition to cardiotoxic drug/radiation
▸Use of diuretics
▸Orthopnoea / paroxysmal nocturnal dyspnoea
▸2. Physical examination:
▸Rales
▸Bilateral ankle oedema
▸Heart murmur
▸Jugular venous dilatation
▸Laterally displaced/broadened apical beat
▸3. ECG:
▸Any abnormality

ASSESSMENT OF HEART FAILURE
PROBABILITY
▸1. Clinical history; 2. Physical examination; 3. ECG
▸≥1 present
▸NATRIURETIC PEPTIDES
▸NT-proBNP ≥125 pg/mL
▸BNP ≥35 pg/mL
▸Consider aetiology and start appropriate treatment
▸ECHOCARDIOGRAPHY

ESC HEART FAILURE GUIDELINES
▸Use transthoracic echocardiography in patients with
suspected or established HF for the assessment of
myocardial structure and function along with the
measurement of LVEF to establish the diagnosis of
▸HF with reduced (HFrEF, LVEF<40%),
▸mid-range (HFmrEF, LVEF: 40-49%) or
▸preserved ejection fraction (HFpEF, LVEF≥50%)

CLINICAL CLASSIFICATION

FORRESTER HAEMODYNAMIC SUBSETS -
AHF IN NUMBERS
Subset Description
I: Warm and dry (normal) PCWP 15–18 mmHg and CI >2.2 L/min/m2
II: Warm and wet (congestion) PCWP >18 mmHg and CI >2.2 L/min/m2
III: Cold and dry (hypoperfusion) PCWP 15–18 mmHg and CI <2.2 L/min/m2
IV: Cold and wet (congestion and
PCWP >18 mmHg and CI <2.2 L/min/m2
hypoperfusion)
Forrester Hemodynamic Subsets
CI: cardiac index; PCWP: pulmonary capillary wedge pressure.
Forrester JS, Diamond G, Chatterjee K, et al. Medical therapy of acute myocardial infarction by application of hemodynamic subsets. N Engl J Med. 1976;295:1356–1362.

BEDSIDE TEST - ECG

ECG - INFERIOR STEMI WITH RV INFARCTION
ST elevation in V1 – the only standard ECG lead that looks directly at the right ventricle.
ST elevation in lead III > lead II – because lead III is more “rightward facing” than lead II and hence
more sensitive to the injury current produced by the right ventricle.
Right ventricular infarction complicates up to 40% of inferior STEMIs.
Patients with RV infarction are very preload sensitive (due to poor RV contractility) and can develop
severe hypotension in response to nitrates or other preload-reducing agents.
Hypotension in right ventricular infarction is treated with cautious fluid loading, and nitrates are
contraindicated.

IMAGING IN AHF
▸CXR
▸ECHOCARDIOGRAPHY
▸LUNG ULTRASOUND

RADIOLOGICAL FEATURES OF ACUTE
PULMONARY OEDEMA
▸There are distinct radiological phases.
▸Interstitial phase is the fluid filling up spaces between acini;
▸the alveolar phase is where that fluid floods the air spaces.
▸Interstitial pulmonary oedema may develop first.
▸Small pulmonary vessels lose their definition
▸Peribronchial cuffing occurs:
▸Kerley B lines
▸Thickening of fissures
▸Pleural effusions
▸Bat Wing" oedema
▸15% Normal CXR

RADIOLOGICAL STAGES OF HEART FAILURE

MILD PULMONARY CONGESTION WITH
CEPHALISATION
AP chest radiograph demonstrates cephalisation (upper lobe vascular redistribution) in stage I CCF where
there is elevation of the left atrial pressure 10-15 mmHg. Normal left atrial pressure is 5-10 mmHg.
http://www.radiologyassistant.nl/en/p4c132f36513d

MORE ADVANCED CONGESTION - KERLEY B
LINES
Stage II - Interstitial oedema
Stage II of CHF is characterised by fluid leakage into the interlobular and peribronchial interstitium as a result of the
When fluid leaks into the peripheral interlobular septa it is seen as Kerley B or septal lines.
Kerley-B lines are seen as peripheral short 1-2 cm horizontal lines near the costophrenic angles.
These lines run perpendicular to the pleura.

EVEN MORE ADVANCED CONGESTION
When fluid leaks into the peribronchovascular interstitium it is seen as thickening of the bronchial walls (peribronchial
cuffing) and as loss of definition of these vessels (perihilar haze).
On the left a patient with heart failure.
There is an increase in the caliber of the pulmonary vessels and they have lost their definition because they are

ENDSTAGE - PULMONARY
CONGESTION WITH
CARDIOMEGALY

ULTRASOUND
IS YOUR NEW
STETHOSCOP
E

ECHOCARDIOGRAPHY
▸Primary imaging modality to
evaluate a patient’s cardiac
function and evaluate for
either systolic or diastolic
dysfunction
▸only part of the initial ED
examination where systolic
and diastolic dysfunction can
be distinguished
▸approximation of LVEF
▸visual assessment that looks
for the general quality of the
“heart’s squeeze”

ECHOCARDIOGRAPHY
▸A more precise way to examine left
ventricular ejection fraction is via E-point
septal separation (EPSS),
▸measures the smallest distance between
the tip of the mitral leaflet and the
interventricular septum during diastole.
▸This distance is assessed using M-mode,
with the indicator overlying the tip of the
mitral lea et.
▸The larger this distance, the lower the
ejection fraction. EPSS > 7 mm is
indicative of poor left ventricular
Secko MA, Lazar JM, Salciccioli LA, et al. Can junior emergency physicians use E-point septal
separation to accurately estimate left ventricular function in acutely dyspneic patients? Acad Emerg
Med. 2011;18(11):1223-1226. (Prospective observational study; 58 patients)
Normal
Abnormal
M-Mode

PULMONARY
ULTRASOUND - B LINES
Multiple B-lines from a case of cardiogenic pulmonaryoedema.
When a similar pattern is visualised on multiple locations in the anterior and lateral chest, it
is diagnostic of the interstitial syndrome.
Interstitial
Pulmonary fluid is identifiable on ultrasound as vertical hyper-echoic lines that arise from,
and run perpendicular to, the pleura.
These lines extend into the lung parenchyma and are referred to as B-lines.
The presence of 3 or more B-lines in at least 2 bilateral lung zones is indicative of
pulmonary oedema.
The greater the number of zones demonstrating B-lines, the higher the likelihood ofADHF
Combined with BNP - High Dx accuracy!
Liteplo AS, et al. Emergency thoracic ultrasound in the differentiation of the etiology of shortness of breath (ETUDES): sonographic B-lines and N-terminal pro-brain-type natriuretic peptide in diagnosing congestive heart failure. Aca

INITIAL EVALUATION - LABORATORY
TESTING
▸BNP
▸Troponin
▸FBC
▸U/E’s
▸Supplementary Testing

BNP
▸BNP Cutoff of 100 ng/l,
▸BNP had a sensitivity 90%, specificity 76%, negative predictive 79%, and
positive predictive value of 89%.
▸In this capacity, BNP is highly useful to exclude AHF
▸negative likelihood ratio of BNP at 100 pg/mL is 0.13 -LR
▸< 100 ng/l strongly suggestive against AHF
▸>400ng/l suggestive of AHF exacerbation
• However may be falsely elevated in:
• Renal disease, atrial fibrillation, pulmonary HTN
• May be falsely low in:
• Obese patients, HFPEF
• High BNP increased Mortality in men
1. Maisel AS, et all . Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure. N Engl J Med. 2002;347:161–167.

TROPONIN
▸Useful for risk stratification
▸? underlying primary cause of AHF (cardiac strain,
ischaemia, infarction)
▸elevated trop = increased in hospital mortality 8% versus 2.7
% if Neg Trop
▸increased re-hospitalisation rate
▸increased risk at death at 90 days

FBC, U/E,S + SUPPLEMENTAL TESTS
▸Anaemia- HB under 8 (in IHD under 10)- improve Oxygen
carrying capacity by transfusion
▸Sodium and Renal function (AKI?-end organ damage)
▸Liver function (end organ damage)
▸Thyroid function (cause of failure?)
▸Calcium - low? improves cardiac contractility
▸amyloidosis, pheochromocytoma etc as rare causes.

TREATMENT AIMS
▸Decrease left ventricular diastolic pressure, by decreasing
systemic vascular resistance and improving systolic and
diastolic functional reserve.
▸Promote coronary blood flow.
▸Correct acute respiratory failure.
▸In-hospital mortality for APO is up to 12%, with one-year
mortality up to 40% !

MANAGEMENT OF PRELOAD
▸ Diuretics
▸ Fluid restriction
▸ Venodilators
▸ Aldosterone agonists
▸ Beta-blockers
▸ Maintenance of sinus rhythm and atrial systolic contribution
▸ Pacing to maintain AV synchrony

MANAGEMENT OF AFTERLOAD
▸Left ventricle
▸Vasodilators
▸ACE-inhibitors
▸Beta-blockers
▸Right ventricle
▸Normoxia
▸Normocapnea
▸Avoidance of excessive postive respiratory pressures
▸Pulmonary vasodilators

MANAGEMENT OF CARDIAC CONTRACTILITY
▸ Inotropes
▸Digoxin
▸Dobutamine
▸Levosimendan
▸ Cardiac resychronisation
▸ Supportive hormones and micronutrients (cortisol, insulin, calcium,
glucagon, thyroxine, thiamine etc

DIAGNOSIS AND INITIAL PROGNOSTIC EVALUATION - BE A CHAMP
Jessup, M. et al. (2016) 2016 ESC and
ACC/AHA/HFSA heart failure guideline
update — what is new and why is it
important?
Nat. Rev. Cardiol.
doi:10.1038/nrcardio.2016.134

IDENTIFICATION OF PRECIPITANTS/CAUSES LEADING TO DECOMPENSATION
THAT NEEDS URGENT MANAGEMENT
▸Acute coronary syndrome.
▸Coexistence of these two clinical conditions (ACS and AHF) always identifies a very-high-risk group where an immediate (i.e. <2 h from hospital admission in patients
with NSTEMI, analogous to STEMI management)
▸invasive strategy with intent to perform revascularization is recommended, irrespective of ECG or biomarker findings.
▸Hypertensive emergency.
▸AHF precipitated by rapid and excessive increase in arterial blood pressure typically manifests as acute pulmonary oedema. Aggressive blood pressure reduction (in
the range of 25% during the first few hours and cautiously thereafter) with i.v. vasodilators in combination with loop diuretics is recommended.
▸Rapid arrhythmias or severe bradycardia/conduction disturbance.
▸Severe rhythm disturbances in patients with AHF and unstable conditions should be corrected urgently with medical therapy, electrical cardioversion or temporary
pacing
▸Electrical cardioversion is recommended if an atrial or ventricular arrhythmia is thought to be contributing to the patient's haemodynamic compromise in order to
restore sinus rhythm and improve the patient's clinical condition.
▸Acute mechanical cause underlying AHF.
▸mechanical complication of ACS (free wall rupture, ventricular septal defect, acute mitral regurgitation),
▸chest trauma or cardiac intervention
▸Echocardiography is essential for diagnosis, and treatment typically requires circulatory support with surgical or percutaneous intervention.
▸ • Acute pulmonary embolism. When acute pulmonary embolism is confirmed as the cause of shock or hypotension, immediate specific treatment is recommended with
primary reperfusion either with thrombolysis, catheter-based approach or surgical embolectomy.

CUTE DECOMPENSATED HEART FAILURE
INITIAL
MANAGE
MENT
PATHWAY

5 DISTINCT TREATMENT GROUPS
▸Acute heart failure syndrome (AHFS) spectrum can be divided into 5 groups as
regards therapeutic management:
▸Dyspnoea + /- congestion with elevated systolic blood pressure (SBP)>140
mmHg, usually with abrupt onset APO (most frequent type)
▸Dyspnoea + /- congestion with normal SBP 100-140 mmHg, usually with gradual
onset predominant systemic oedema and milder APO
▸Dyspnoea + /- congestion with low SBP <100 mmHg, with predominant
cardiogenic shock or end-stage cardiac failure (most fatal type)
▸Dyspnoea + /- congestion with signs of ACS such as chest pain
▸Isolated RV failure usually without APO
Mebazza A, Gheoghiade M, Pina I et al. Practical recommendations for prehospital and early in-hospital management of patients presenting with acute heart failure. Crit Care Med 2008;36:S129-39.

CLINICAL CLASSIFICATION
Classification of patients presenting with acutely decompensated heart failu
Yancy C W et al. Circulation.2013;128:e240-e327

PRACTICAL RECOMMENDATION
Alexandre Mebazaa, MD, PhD et all “Practical recommendations
for prehospital and early inhospital management of patients
presenting with acute heart failure
syndromes” Crit Care Med 2008 Vol. 36, No. 1

VASODILATORS
▸ Safety of high dose initial GTN:
▸ 800 mcg(2x0,4mg sl tab) GTN sl if BP>180mmHg
▸ 1200 mcg(3x0.4mg sl Tab) for BP>200 mmHg
▸ only 3/75 incidence of Hypotension
▸ Initial GTN dose iv 50-100mcg/min up to 400mcg/min for 2 min max with Physician
in attendance
▸ Vasodilators should be used with extreme caution in patients with significant mitral
or aortic stenosis.
Clemency BM, Thompson JJ, Tundo GN, et al.
Prehospital Disaster Medicine high-dose
sublingual nitroglycerin rarely causes hypotension.
Prehosp Disaster Med. 2013;28(5):477-481.
(Retrospective cohort study; 75 patients)

VASODILATORS
‣ No robust evidence confirming their beneficial effects.
‣ They have dual benefit by
‣ decreasing venous tone (to optimize preload)
‣ decreasing arterial tone (decrease afterload).
‣ they may also increase stroke volume.
‣ Vasodilators are especially useful in patients with hypertensive AHF, whereas in SBP <90 mmHg (or with s

INOTROPIC AGENTS
▸ Digoxin - no improvement over placebo in one (older) study
▸ Dopamine was compared with norepinephrine in the treatment of various shock patients.
▸ Increased Mortality
▸ A subgroup analysis suggested that norepinephrine would have fewer side effects and lower mortality
▸ Norepinephrine 1st choice but increasing Oxygen demand in Heart
De Backer D , Biston P, Devriendt J, Madl C, Chochrad D, Aldecoa C, Brasseur A, Defrance
P, Gottignies P, Vincent J-L. Comparison of dopamine and norepinephrine in the treatment of
shock. N Engl J Med 2010;362:779–789.

INOTROPES

DIGOXIN
▸Digoxin is if at all indicated in patients with AF and rapid
ventricular rate (>110 bpm)
▸boluses of 0.25–0.5 mg i.v. if not used previously

MANAGEMENT OF PATIENTS WITH CARDIOGENIC SHOCK
▸Pharmacologic therapy aims to improve organ perfusion
▸by increasing cardiac output and blood pressure.
▸fluid challenge,
▸inotropic agent (Dobutamine)and a
▸vasopressor (noradrenaline) as needed.
▸immediate Coronary Angiogram recommended

DIURETICS
▸Diuretics are a cornerstone in the treatment of patients with AHF and signs of fluid overload and
congestion.
▸Diuretics increase renal salt and water excretion and have some vasodilatory effect.
▸In patients with AHF and signs of hypoperfusion, diuretics should be avoided before adequate perfusion
is attained.
▸The initial approach to congestion management involves i.v. diuretics with the addition of vasodilators for
dyspnoea relief if blood pressure allows.
▸Options include dual nephron blockade by loop diuretics (i.e. furosemide or torasemide) with thiazide
diuretics or natriuretic doses of MRAs
▸Administration of furosemide at 2.5 times the previous oral dose resulted in greater improvementin
dyspnoea, larger weight change and fluid loss at the cost of transient worsening in renalfunction.
▸patients with new-onset AHF or those with chronic HF without a history of renal failure and previous use
of diuretics may respond to i.v. boluses of 20–40 mg

FURUSEMIDE
Felker GM , Lee KL, Bull DA, Redfield MM, Stevenson LW, Goldsmith SR, LeWinter MM,
Deswal A, Rouleau JL, Ofili EO, Anstrom KJ, Hernandez AF, McNulty SE, Velazquez EJ,
Kfoury AG, Chen HH, Givertz MM, Semigran MJ, Bart BA, Mascette AM, Braunwald E,
O'Connor CM. Diuretic strategies in patients with acute decompensated heart failure. N EnglJ
Med 2011;364:797–805.
▸In Patient with Evidence of Fluid overload Diuretics to be started
early in ED stay
▸In the ‘high-dose’ arm of the DOSE study, administration of
furosemide at 2.5 times the previous oral dose resulted in
greater improvement in dyspnoea, larger weight change and
fluid loss at the cost of transient worsening in renal function
▸i.v. Furusemide should be given at least the same or larger
the daily po dose to improve outcomes.
▸starting does for Furusemide in de move patients 20-40mg iv

OXYGEN
▸In AHF, oxygen should not be used routinely in non-
hypoxaemic patients, as it causes vasoconstriction and a
reduction in cardiac output.
▸In COPD, hyperoxygenation may increase ventilation–
perfusion mismatch, suppressing ventilation and leading to
hypercapnia.
▸During oxygen therapy, acid–base balance and
transcutaneous SpO2 should be monitored.
Park JH , Balmain S, Berry C, Morton JJ, McMurray JJV. Potentially detrimental
cardiovascular effects of oxygen in patients with chronic left ventricular systolic dysfunction.
Heart 2010;96:533–538.

OPIATES…RATHER USE BENZO’S
▸Opiates relieve dyspnoea and anxiety.
▸In AHF, routine use of opiates is not recommended and they may
only be cautiously considered in patients with severe dyspnoea,
mostly with pulmonary oedema.
▸Dose-dependent side effects include nausea, hypotension,
bradycardia and respiratory depression (potentially increasing the
need for invasive ventilation).
▸There are controversies regarding the potentially elevated
mortality risk in patients receiving morphine
Peacock WF , Hollander JE, Diercks DB, Lopatin M, Fonarow G, Emerman CL. Morphineand
outcomes in acute decompensated heart failure: an ADHERE analysis. EmergMed
J 2008;25:205–209.

LEVOSIMENDAN
▸“Calcium-sensitiser”
▸works by increasing myocardial contractility
▸by sensitising the cardiac myocytes to calcium
▸ In the REVIVE study levosimendan, when added to standard therapy,
resulted in a more rapid symptomatic improvement when compared to
placebo with standard therapy;
▸increased risk of hypotension and dysrhythmias associated with its
administration
Packer M, Colucci W, Fisher L, et al. Effect of Levosimendan on the
short term clinical course of patients with acutely decompensated heart
failure. JACC Heart Fail2013;1(2):103- 111. (Randomized controlled trial;
700 patients

VENTILATORY ASSISTANCE
▸ Non-invasive ventilation (NIV) refers to CPAP; or bilevel positive airway pressure
(BiPAP) non-invasive pressure support ventilation (NIPSV), where IPAP – EPAP
(≡PEEP) reflects the amount of pressure support delivered.
▸CPAP reduces mortality (RR 0.64) and need to intubate (RR 0.44), with no effect
on incidence of new MI. BiPAP reduces need to intubate (RR 0.54), but not
mortality or new MI. Thus CPAP preferred in APO due to AMI / ischaemia.
▸Note 3CPO trial findings showed negative effect of NIV compared to standard
medical therapy alone, but may be explained by sickest patients were excluded,
low overall rates of intubation, ischaemia and mortality (i.e. their patients were
different), and considerable treatment group crossover after first 2 hours.

NIV
▸Non-invasive positive pressure ventilation includes both CPAP and bi-level positive
pressure ventilation (PPV). Bi-level PPV also allows inspiratory pressure support that
improves minute ventilation and is especially useful in patients with hypercapnia, most
typically COPD patients.
▸Non-invasive positive pressure ventilation includes both CPAP and bi-level positive
pressure ventilation (PPV). Bi-level PPV also allows inspiratory pressure support that
improves minute ventilation and is especially useful in patients with hypercapnia, most
typically COPD patients.
▸Non-invasive positive pressure ventilation reduces respiratory distress and may decrease
intubation and mortality rate
▸In one study (Emerg Med J 2004; 21:155-161) survival to hospital discharge was improved
with CPAP (10 mm/Hg) over BiPap (Ipap 15 Epap 5) and conventional therapy
Vital FMR , Ladeira MT, Atallah AN. Non-invasive positive pressure ventilation (CPAP or
bilevel NPPV) for cardiogenic pulmonary oedema. Cochrane DatabaseSyst
Rev 2013;5:CD005351.

EARLY REVASCULARISATION THERAPY IN
ISCHAEMIC ECG
▸The SHOCK Trial showed a 67% relative improvement in
long-term survival, measured at 6 years, for patients
managed with rapid revascularization.
▸Role of revascularization is not clear for patients presenting
with failure without obvious acute ischemia.
Hochman JS, Sleeper LA, Webb JG, et al. Early revascularization andlong-
term survival in cardiogenic shock complicat- ing acute myocardialinfarction.
JAMA. 2006;295(21):2511- 2515. (Randomized controlled trial; 302patients)

ULTRAFILTRATION
▸Ultrafiltration is similar to hemodialysis; however, it focuses on
fluid removal rather than solute exchange.
▸can be accomplished through a smaller-diameter catheter than
hemodialysis, but it generally requires a peripherally inserted
central catheter (PICC) line
▸The UNLOAD trial evaluated ultrafiltration versus IV diuretic
therapy in patients with functioning kidneys, and it demonstrated
that ultrafiltration removes a larger volume of fluid and is
associated with a greater reduction in 90-day resource utilisation
compared to diuretic therapy.

MANAGEMENT OF PATIENTS WITH ACUTE
HEART FAILURE

INITIAL MANAGEMENT OF A PATIENT WITH
ACUTE HEART FAILURE
Jessup, M. et al. (2016) 2016 ESC and ACC/AHA/HFSA heart failure guideline update — what is new and why is it important?
Nat. Rev. Cardiol. doi:10.1038/nrcardio.2016.134
Modified from Ponikowski, P. et al. 2016 ESC guidelines for the diagnosis and treatment of acute and chronic heart
failure: the Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of
Cardiology (ESC). Developed with the special contribution of the Heart Failure Association (HFA) of the ESC.
Eur. Heart J. http://dx.doi.org/10.1093/eurheartj/ehw128 (2016), with permission from Oxford University Press and the ESC

MECHANICAL RESCUE DEVICES AND
CHEATS
▸Increase cardiac output by unnatural means:
▸LVAD
▸ECMO
▸Increase the pacemaker rate (60-90 increase of CO by 30%)
▸Decrease the organism's demand for cardiac output
▸Hypothermia
▸Paralysis/sedation

BRIDGING THERAPY TO HEART
TRANSPLANT ?

TEXT
OPIATES
▸Opiates relieve dyspnoea and anxiety.
▸In AHF, routine use of opiates is not recommended
▸only be cautiously considered in patients with severe dyspnoea, mostly
with pulmonary oedema.
▸Dose-dependent side effects
▸nausea, hypotension, bradycardia and respiratory depression
(potentially increasing the need for invasive ventilation).
▸There are controversies regarding the potentially elevated mortality
risk in patients receiving morphine
Iakobishvili et all, Use of intravenous morphine for acute decompensated heart failure in patients with and without acute coronary syndromes.
Acute Card Care 2011;13:76–80.
PeacockWF.ett all.Morphine and outcomes in acute decompensated heart failure: an ADHERE analysis.Emerg Med J
2008;25:205–209.

DEVICE THERAPY - RRT
▸Renal Replacement Therapy - routine use of ultrafiltration is not
recommended
▸Criteria for initiation of renal replacement therapy in patients with refractory
volume overload:
▸oliguria unresponsive to fluid resuscitation measures,
▸severe hyperkalaemia (K+ >6.5 mmol/L),
▸severe acidaemia (pH <7.2),
▸serum urea level >25 mmol/L (150 mg/dL) and
▸serum creatinine >300 µmol/L (>3.4 mg/dL)

DEVICE THERAPY - MECHANICAL ASSIST
DEVICES
▸Intra-aortic balloon pump
▸in cardiac shock
▸otherwise no good evidence
▸ IABP did not improve outcomes in patients
suffering from AMI and cardiogenic shock -
(IABP-SHOCK II trial)
▸Left Ventricular assist devices (LVAD)
▸ (MCS) may be used as a ‘bridge to
decision’ or longer term in selected
patients
Thiele H. et all.Intra-aortic balloon counterpulsation in acute myocardial infarction complicated by cardiogenic shock (IABP-SHOCK II): final 12 month results of a randomised, open-label trial. Lancet 2013

OTHER INTERVENTIONS
▸In patients with AHF and pleural effusion, pleurocentesis
with fluid evacuation may be considered if feasible in order
to alleviate dyspnoea.
▸In ascites, ascitic paracentesis with fluid evacuation may be
considered in order to alleviate symptoms.
▸reduction in intra-abdominal pressure,
▸partially normalizes the transrenal pressure gradient, thus
improving renal filtration.

DISPOSITION
▸The criteria for ICU/CCU admission include any of the following:
▸ need for intubation (or already intubated)
▸ signs/symptoms of hypoperfusion
▸ oxygen saturation (SpO2) <90% (despite supplemental
oxygen)
▸ use of accessory muscles for breathing, respiratory rate
>25/min
▸ heart rate <40 or >130 bpm, SBP <90 mmHg.

CLINICAL VIGNETTE - OUTCOME OF YOUR
PATIENT
▸ The middle-aged man with hypertensive decompensated heart
failure with acute pulmonary oedema, was started immediately
on BiPAP to support his breathing, and he responded well.
Bedside pulmonary ultrasound showed B-lines, confirming the
diagnosis of pulmonary oedema. He was started on a high-dose
nitroglycerin drip, which resulted in a significant improvement in
his respiratory symptoms. He received IV diuresis and was
admitted to the ICU for further management.

TEXT
TAKE HOME MESSAGE - BE A CHAMP

USEFUL SCRIPTURE
▸EBMEDICINE Acute Decompensated Heart Failure: New Strategies
for Improving Outcomes May 2017
▸2016 ESC Guidelines for the diagnosis and treatment of acute and
chronic heart failure: The Task Force for the diagnosis and treatment
of acute and chronic heart failure of the European Society of
Cardiology (ESC)Eur Heart J (2016) 37 (27): 2129-2200

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