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ACUTE DECOMPENSATED

HEART FAILURE
From Hemodynamic Subset to Appropriate Treatment

Budi Baktijasa

Riana Handayani, MD
Definition
Stage A High risk with no symptom
Stage B Structural heart disease, with no symptom
Stage C Structural heart disease, with previous or
current symptom
Stage D Refractory symptoms requiring special
intervention

ACC AHA Guidelines 2009


Stages of HF: ACC/AHA
Stage A
High Risk for developing
Heart failure

Stage B
Asymptomatic
LV dysfunction NYHA Functional Class
Class I
symptoms at activity levels that
would limit normal individuals
Stage C Class II
Past or current symptoms of HF with
ordinary exertion
Symptoms of HF Class III
symptoms of HF with less
than ordinary exertion

Stage D Class IV
End-stage HF Symptoms of HF at rest

ACC AHA Guidelines 2009


EVOLUTION OF
CLINICAL STAGES

NORMAL
NORMAL
No
No Asymptomati
Asymptomati
symptoms
symptoms c
c LV
LV
Normal
Normal
exercise Dysfunction
Dysfunction
exercise
Normal
Normal LV
LV
No
No
symptoms
symptoms
Compensate
Compensate
function
function Normal
Normal d
d CHF
CHF
exercise
exercise No
No Decompensate
Decompensate
Abnormal LV
Abnormal LV symptoms
symptoms
function
function Exercise d
Exercise d CHF
CHF
Abnormal
Abnormal LVLVSymptoms
Symptoms Refractory
Refractory
function
function Exercise
Exercise
Abnormal
Abnormal LV
CHF
LV CHF
function
function Symptoms
Symptoms not
not
controlled
controlled with
with
treatment
treatment
Terminology
Final Common Pathway in Heart Failure
Diagnosis of ADHF

• Harder
Many thanconditions
you think may mimic HF
• Even
Need cardiologists
to practice,get itpractice,
wrong sometimes
practice
• No single finding is definitive
Need to integrate all the findings (history, exam,
labs, CXR, EKG)
Clinical Classification of AHF

HYPERTENSIVE
AHF
ACUTELY
DECOMPENSATED
CHRONIC HF

PULMONARY
OEDEMA
ACS AND
HF
CARDIOGENIC RIGHT HF
SHOCK

European Heart Journal (2008) 29, 2388–2442


Signs and Symptom of ADHF
Hypotension
Cool extremities
Narrow pulse pressure Low
Sleepiness, obtundation Perfusion
Elevated BUN, creatinine
Hyponatremia

Orthopnea
Paroxysmal Nocturnal Dyspnea
Neck vein distention
Congestion Ascites, edema
Hepatojugular Reflux
Stevenson LW. Eur J Heart Fail.Rales
1999;1:251
Primary goal in making diagnosis:
Discovering signs and symptoms of high
right and left atrial pressures
The most reliable signs for elevated left-
sided filling pressures then are the
presence of an elevated JVP (>7 cmH2O)
or positive abdominojugular reflux (AJR)
Clinical Application

Hemodynamic Profile in
2
Minutes
Hemodynamic State of AHF
Evidence For Congestion
Orthopnea Edema
High Jugular Venous Pressure Ascites
Increasing S3 Rales
Loud P2 Abdominojugular reflux

Evidence for Low Congestion at Rest


Perfusion NO YES

Low Perfusion at Rest


•Narrow Pulse Pressure
•Pulsus Alternans
•Cool Forearms and Legs NO
•Sleepy, Obtunded
•ACE-inhibitor related
Symptomatic Hypotension
•Declining Serum Sodium Level YES
•Worsening Renal Function

Nohria A, Lewis EF and Stevenson LW. Medical Management of advanced heart failure.JAMA.2002;287:629
Hemodynamic
profiles
Relative Risk (95% CI)
(457) Ref

(255) 2.304 (1.303-4.076)

(15) 5.803 (1.992-16.906)

(15) 8.705 (3.513-21.567)

n = 742 No. of patients

ICVCU Harapan Kita Hospital Registry, Asia Pacific Society of Cardiology Congress Pattaya
2012
n = 560

*
* Mean Differences:
* •Dry-Warm Ref
•Wet-Warm 1.719
•Dry-Cold 3,418
•Wet-Cold 4,654

* = p < 0.001

ICVCU Harapan Kita Hospital Registry, Asia Pacific Society of Cardiology Congress Pattaya
2012
Hemodynamic Profiles & Mortality
Six-months mortality by clinically determined hemodynamic profiles

6-mths
Patient Profile N (%)
mortality (%)
Dry – Warm (A) 123 (27) 11
Wet – Warm (B) 222 (49) 22
Wet – Cold (C) 91 (20) 40

Dry – Cold (L) 16 (4) 17

Nohria A, et al. J Am Coll Cardiol 2003;41:1797-1804


Etiology of Shock
1. Hypovolemic - intravascular fluid volume loss
(dehydration, haemorhagic, diuretic)

3. Obstructive - factors extrinsic to cardiac valves and


myocardium (Tamponade)

2. Cardiogenic - impairment of heart pump

4. Distributive - pathologic redistribution of intravascular


fluid volume (septic, anaphylactic)
HEMODYNAMIC PROFILE
OF SHOCK

LOW PERFUSION CONGESTION


•Blood Pressure , •Auscultation
• Cardiac Output < 3.2 l/mnt •orthopnue
•PCWP > 18 mmHg

COLD DRY or WET


HEMODYNAMIC PROFILE
OF SHOCK
LOW PERFUSION
(COLD)

WITHOUT CONGESTION
WITH CONGESTION Hypovolemic
(Cardiogenic Shock) Distributive shock (septic, anafilactic)
COLD-WET RV Failure
COLD-DRY
Treatment Goals

Relieve symptoms and signs


Prevent hospital admission,
Improve survival

ESC Guidelines 2012


Treatment
Algorithm

ESC Guidelines 2012


Escalating Therapy for Heart Failure as Symptomatic Status Progresses

TREATING HEMODYNAMIC PROFILES

Dry Wet

Warm
A B Diuretics
Vasodilators:
Natriuretic peptides
Nitroprusside
Cold
L C Nitroglycerin

Inotropic Drugs
Dobutamine
Milrinone
Levosimendan
Enoximone

Stevenson L W Eur J Heart Fail 2005;7:323-331


Fluid Diuretics
Retension

Agents that alter the physiological renal


mechanisms that form urine in such a way that
there is increased flow of urine with greater
excretion of sodium (natriuresis)

Control pulmonary and peripheral symptoms


Control sign of congestion
Classification of Diuretics
(for Heart failure Management)

Potassium
Loop Thiazides/
Sparing
diuretics Thiazides-like
Diuretics

Furosemide Hydrochlorthiazid Spironolactone


Bumetanide Chlortalidone Amiloride
Torsemide Indapamid Triamterene
Metolazone Eplerenone
Etacrynic acid
Loop Diuretics Act at defferent
tubular sites

Thiazide

K Sparing
Diuretics
Additive effect
Cardiac Output :
Stroke Volume x Heart Rate

Maintaining Stroke Volume :

- Maintaining Contractility ~
Neurohormonal
(sympathetic and Vagal)
- Maintaining Preload ~ Frank-Starling
Law of The
Heart
Failing Heart

Preload Contractility Afterload

Stroke Volume
Failing Heart
Diuretics ACEi ARB
Nitrates Beta bloker

Preload Contractility Afterload

Digitalis
intotropes
Vasodilators ( Nitroglycerin )

Preload reduction
Vasodilation effect  lowers preload
reduce pulmonary congestion
Should be avoided : Systolic blood
pressure <110 mmHg
Opiates

Reduce the anxiety associated with


dyspnea
Venodilators  reduce preload
Reduce sympathetic drive
Depress respiratory drive
Increasing the need for invasive
ventilation
Vasopressors and Inotropes in Acute Heart Failure
Bolus Infusion Rate
Dobutamine No 2 – 20 mcg/kg/mnt
Dopamine No <3 mcg/kg/mnt : renal effect
3 – 5 mcg/kg/mnt : inotropic
>5 mcg/kg/mnt : vasopressor
Milrinone 25 – 75 mcg/kg over 10-20 0.375 – 0.75 mcg/kg/mnt
mnt
Enoximone 0.5 – 1 mcg/kg over 5-10 mnt 5 – 20 mcg/kg/mnt
Levosimendan 12 mcg/kg over 10 mnt 0.1 mg/kg/mnt (can be
(optional) decreased to 0.05 mcg/kg/mnt
or increased to 0.2
mcg/kg/mnt)
Norephinephrine No 0.2 – 1 mcg/kg/mnt
Ephinephrine Bolus 1 mg can be given i.v 0.05 – 0.5 mcg/kg/mnt
during resucitation, repeated
every 3 – 5 mnt

ESC Guidelines 2012


Location and Effect of
Stimulation Cathecolamine
Receptors
Inotropes Vs
Vasopressors

VS
Inotropes

 Drugs that affect


the force of
contraction of
myocardial muscle
 Positive or negative
 Term “inotrope”
generally used to
describe positive
effect
Vasopress
or

 Drugs that
stimulates smooth
muscle contraction
of the capillaries &
arteries
 Cause
vasoconstriction &
a consequent rise
in blood pressure
Mixed action Inotropic +
Vasopressor
Main Goal

Tissue perfusion &


oxygenation
Physiological Principles
MAP = CO x SVR
~ 1
r4
CO = HR x SV
Preload Contractility Afterload
Basic principles -
Vasopressors
MAP = CO x SVR
~ 1
r4
CO = HR x SV
Preload Contractility Afterload
Basic principles - Inotropes
MAP = CO x SVR

CO = HR x SV
Preload Contractility Afterload
Which adrenoceptor mediates
cardiac muscle contraction?

1. 1
2. 2
3. 1
4. 2
Which adrenoceptor mediates
vascular smooth muscle
contraction?

1. 1
2. 2
3. 1
4. 2
Main classes of
Adrenoceptor
  receptors
 1
 Located in vascular smooth muscle
 Mediate vasoconstriction

 2
 Located throughout the CNS, platelets
 Mediate sedation, analgesia & platelet aggregation
Main classes of
Adrenoceptor
  receptors
 1
 Located in vascular smooth muscle
 Mediate vasoconstriction

 2
 Located throughout the CNS, platelets
 Mediate sedation, analgesia & platelet aggregation
Main classes of
Adrenoceptor
  receptors
 1
 Located in the heart
 Mediate increased contractility & HR

 2
 Located mainly in the smooth muscle of bronchi
 Mediate bronchodilatation
Main classes of
Adrenoceptor
  receptors
 1
 Located in the heart
 Mediate increased contractility & HR

 2
 Located mainly in the smooth muscle of bronchi
 Mediate bronchodilatation
 Located in blood vessels
 Dilatation of coronary vessels
 Dilatation of arteries supplying skeletal muscle
Epinephrine
 Stimulates  &  receptors
 Predominantly  effects at low doses and 
effects at high doses

 Clinical uses
 Cardiac arrest
 Anaphylaxis
 Low cardiac output states
Norepinephrine
 Predominantly stimulates 1 receptors
 Most commonly used vasopressor in
critical care
 Very potent
 Administered by infusion into a central
vein
 Uses
 Hypotension due to vasodilatation
 Septic shock
Dopamine
 Effect dose dependent
 Direct
 Low dose - 1
 High dose - 1
 Indirect
 Stimulates norepinephrine release

 D1 receptors
 Vasodilatation of mesenteric & renal circulation
Dobutamine
 Synthetic
 Predominantly 1

 Small effect at 2
 Uses
 Low cardiac output states
 Cardiogenic shock
Intra Aortic Balloon Pump

•Sudden inflation moves blood superiorly


and inferiorly to the balloon increasing
perfusion to the heart and distal organs
(brain, kidneys, tissues, etc.)
•When the balloon is suddenly deflated,
the pressure within the aorta drops
quickly
INOTROPIC COMPARISON
Harapan Kita Hospital
Non-pharmacologic Therapy
 Restrict sodium intake to < 2 g/day
 Restrict fluid intake to <1.5 – 2.0 L/day
 Ventilation : Continuous positive airway pressure (CPAP) and non-
invasive positive pressure ventilation (NIPPV) to relieve dyspnoea
and improve certain physiological measures (e.g. oxygen saturation)
in patients with acute pulmonary oedema
 Intra-Aortic Balloon Pump (IABP) to support the circulation before
surgical correction of specific acute mechanical problems (e.g. ISR
and acute MR), during severe acute myocarditis and in selected
patients with acute myocardial ischaemia or infarction before, during,
and after percutaneous or surgical revascularization
 Ultrafiltration

ESC Guidelines 2012


HFSA 2010 Practice Guideline
Acute HF—Table 12.4. Patient Monitoring*
Frequency Value Specifics
At least daily Weight Determine after voiding in the morning
Account for possible increased food intake due to
improved appetite
At least daily Fluid intake
and output
More than Vital signs Orthostatic blood pressure, if indicated
daily
Oxygen saturation daily until stable
At least daily Signs Edema, ascites, pulmonary rales, hepatomegaly,
increased jugular venous pressure, hepatojugular reflux,
liver tenderness
At least daily Symptoms Orthopnea, paroxysmal nocturnal dyspnea or cough,
nocturnal cough, dyspnea, fatigue, lightheadedness
At least daily Electrolytes Potassium, sodium

At least daily Renal function BUN, serum creatinine

*All Recommended, Strength of Evidence = C


Acute Heart Failure
After stabilization
Pharmacological Management
Prognosis Symptoms
• Ace inhibitors • Diuretics
• Beta blokers • Digoxin
• Mineralocorticoid • Nitrates
Receptor Antagonist • Ivabradine
• ARB
Non Pharmacology Management

• Risk factor controls (DM, HT, dyslipidemia)


• Risk factor reductions (CHD, RHD, kemotx,
drugs, exercise)
• Family and patient education
• Device/surgical
Device/Surgical Management
Device Surgery
• Simple pace make • Valve
• Biventricular pace repair/replacement
maker • Revascularisation
• Defibrillator • Transplantation
• LV assist devices
ESC Guideline for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2012
ESC Guideline for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2012
ACE Inhibitors
IA
ACE inhibitor is recommended,
in addition to a beta-blocker,
for all patients with an EF ≤40%
to reduce the risk of HF hospitalization
And the risk of premature death.

Angiotension II Receptor Blockers usually used in ACE


intolerant patients

ESC Guideline for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2012
Dose of ACE Inhibitor/ARB
Drugs Starting Dose Target Dose
Captopril 6.25 mg t.i.d 50 mg t.i.d
Enalapril 2.5 mg b.i.d 10 – 20 mg b.i.d
Lisinopril 2.5 – 5 mg OD 20 – 35 mg OD
Ramipril 2.5 mg OD 5 mg OD
Trandolapril 0.5 mg OD 4 mg OD
Candesartan 4 or 8 mg OD 32 mg OD
Valsartan 40 mg b.i.d 160 mg b.i.d
Losartan 50 mg OD 150 mg OD

ESC Guideline for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2012
Trials of ACE Inhibitor in Heart Failure

Avoid stopping ACEI because of cough


Beta-Blocker

IA
A beta-blocker is recommended,
in addition to an ACE inhibitor (or ARB if
ACE inhibitor not tolerated),
for all patients with an EF ≤40%
to reduce the risk of HF hospitalization
and the risk of premature death

ESC Guideline for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2012
Dose of Beta Blockers
Agent Starting Dose Target Dose

Bisoprolol 1.25 mg OD 10 mg OD

Carvedilol 3.125 b.i.d 25 – 50 mg b.i.d

Metoprolol Succinate
12.5 / 25mg OD 200 mg OD
(CR/XL)

Nebivolol 1.25 mg OD 10 mg OD

ESC Guideline for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2012
Trials of B-Blockers in Heart
Failure
Aldosterone Receptor Antagonist

IA
An MRA is recommended for all patients with persisting
symptoms (NYHA class II–IV) and an EF ≤35%,
despite treatment with an ACE inhibitor
(or an ARB if an ACE inhibitor is not tolerated)
and a beta-blocker, to reduce the
risk of HF hospitalization and
the risk of premature death

ESC Guideline for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2012
Dose of MRA
Agent Starting Dose Target Dose

Eplerenone 25 OD 50 mg OD

Spironolactone 25 mg OD 25 – 50 mg OD

ESC Guideline for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2012
Spironolactone in Heart Failure
Ivabradine
• Inhibits If current in SA node
• Slow heart rate in sinus rhytm
• Higher heart rate is associated with higher
mortality in heart failure
Ivabradine
• Should be considered to reduce the risk of HF
hospitalization in patients in sinus rhythm with an EF
≤35%, a heart rate remaining ≥70 b.p.m., and
persisting symptoms (NYHA class II–IV) despite
treatment with an evidence-based dose of beta-
IIa B
blocker (or maximum tolerated dose below that),
ACE inhibitor (or ARB), and an MRA (or ARB)
• May be considered to reduce the risk of HF
hospitalization in patients in sinus rhythm with an EF
≤35% and a heart rate ≥70 b.p.m. who are unable to
tolerate a beta-blocker. Patients should also receive IIb C
an ACE inhibitor (or ARB) and an MRA (or ARB)

ESC Guideline for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2012
ESC Guidelines 2012
Digoxin: Improvement in symptoms but not survival
Death or hospitalization for
worsening HF
• Digitalis investigation
group
• 6800 patients
• EF<45%
• Past or current All-cause mortality
symptoms of HF
• On ACEI and diuretics

ESC Guidelines 2012


NEJM 1997;336:525.
Digoxin
IIb B

May be considered to reduce the risk of HF hospitalization


in patients in sinus rhythm with an EF ≤45% who are
unable to tolerate a beta-blocker.
Patients should also receive an ACE inhibitor (or ARB)
and an MRA (or ARB)

ESC Guideline for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2012
Diuretics
• The effects of diuretics on mortality and
morbidity have not been studied in patients with
HF
• The aim of using diuretics is to achieve and
maintain euvolaemia (the patient’s ‘dry weight’)
with the lowest achievable dose

ESC Guidelines 2012


Dose of Diuretics

ESC Guideline for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2012
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