Acute Heart Failure

Prof univ dr Ion C.intoiu

Acute Heart
Failure

Prof univ dr Ion C.intoiu

Objectives

Definitions
Epidemiology
Pathophysiology
Diagnosis
Management
Summary of Guidelines
Recommended Reading

Definitions
Epidemiology
Pathophysiology
Diagnosis
Management
Summary of Guidelines
Recommended Reading

The definition of acute heart

failure has not been firmly
established ().

It is recognized when symptoms of

heart failudevelop rapidly within
hours and
days in patients without prior
evidence of cardiac
decompensation

Acute Heart Failure

Rapid onset of symptoms and signs
related to abnormal cardiac function
As a result of Systolic Dysfunction,
Diastolic Dysfunction, Arrhythmias, or
Preload-After load Mismatch

Acute heart failure

AHF: The rapid onset of symptoms and signs secondary to
abnormal
cardiac function.
(reduced CO, tissue hypoperfusion + congestion, increase in PCWP)
1.
2.

3.

With or without previous cardiac disease.

The cardiac dysfunction can be related:
a) to systolic or diastolic dysfunction
b) to abnormalities in cardiac rhythm
c) to preload and afterload mismatch
Often life threatening and requires urgent treatment.

The Task Force on Acute Heart Failure of the European Society of

Cardiology

ESC Guidelines, 2005

DEFINITION
Rapid onset of symptoms and signs secondary to
abnormal cardiac
function. It may occur with or without
previous cardiac disease.
The cardiac dysfunction can be related to
systolic or diastolic dysfunction,abnormalities in
cardiac rhythm or to pre-load and after load
mismatch

Acute heart failure is heterogeneous

syndrome
Right Heart Failure

PULMONARY
EDEMA
Acute
Decompensated
CHF

Cardiogenic
shock

High Output Failure

Hypertensive HF

Filippatos 2005

Overview: Acute Heart Failure

Complex syndrome caused by

impaired cardiac function

2 types:
left ventricular systolic
dysfunction (LVSD)
Heart failure with preserved
ejection fraction
(HFPEF/HFNEF/Diastolic
dys.)

Commonest cause(s):
IHD, Hypertension, alcohol,
cytotoxics

3040% of patients die within a

year of diagnosis

Expected to rise in the future

The cardiac dysfunction

may be related to
Ischaemia
Arrhythmias
Valvular dysfunction
Pericardial disease
Increased filling
pressures
Elevated systemic
resistance.

Definitions
Epidemiology
Pathophysiology
Diagnosis
Management
Summary of Guidelines
Recommended Reading

Acute heart failure

Epidemiology

1.
2.

Increase of pts with CHF (aging of population + improved

survival) = increase in the number of hospitalisations for the
decompensated heart failure .
Poor prognosis: AMI + SHF: 30% annual mortality
APO: 40% annual mortality
12% in-hospital mortality
CAD: 60-70% (particularly in elderly population)
Dilated cardiomyopathy, arrhythmia, congenital or VHD or
myocarditis: in youmger subjects.

The Task Force on Acute Heart Failure of the European Society of Cardiology

Definitions
Epidemiology
Pathophysiology
Diagnosis
Management
Summary of Guidelines
Recommended Reading

Pathophysiology
LV dysfunction:
Accumulation of fluid.
Decrease in CO
Hypoperfusion.
Reciprocal Activation of (RAAS)
Na, water retention.
AGII
ET1 + Vasopressin.
Reflex activation of SNS: Epi, NE.

A Vicious Circle

Natural history of congestive heart

failure
Normal heart

Chronic heart failure

5 million in the US
10 million in Europe

Initial
myocardial
injury

Heart Viability

Death

First ADHF episode:

Pulmonary edema
ER admission

Later ADHF episodes:

Rescue therapy
ICU admission

Initial phase

Last year
Gheorghiade M. Am J Cardiol. 2005;96(suppl 6A):1-4G.

Ventricular function

Acute Exacerbations May Contribute to

the Progression of the Disease
With each event,
hemodynamic alterations
contribute to progressive
ventricular dysfunction.

Acute event

Time
Gheorghiade M, Fonarow G, Filippatos G et al. Am J Cardiology 2005

Initial and Serial Evaluation of

the AHF Patient

Clinical CLASIFICATION

Acute Heart Failure : Classification

Can present itself as:

Acute de novo (new onset of AHF in a patient

without
previously
known
cardiac
dysfunction).
or
Acute decompensation of chronic heart
failure.
The Task Force on Acute Heart Failure of the European Society of Cardiology

Killip Classification
Stage I:
No clinical signs of decompensation.
Stage II:
Heart failure. Rales, S3, PVH.
Stage III:
Severe heart failure. Pulmonary edema with rales
throughout the lung fields.
Stage IV:
Cardiogenic Shock: Hypotension, peripheral
vasoconstriction, oliguria, cyanosis and diaphoresis.

Forrester Classification
Cardiac Index
(L/min/m2)
5
4

18 mmHg

Subset I
(Normal)
Warm and Dry

Subset II
(Congestion)
Warm and Wet

Subset III
(Hypoperfusion)
Cold and Dry

Subset IV
(Congestion and
hypoperfusion)
Cold and Wet

3
2.2L/min/m2

2
1

10

20

Pulmonary Capillary Wedge Pressure (mmHg)

30

Nohria A et al. JAMA.2002:287; 628-40

Acute Heart Failure :

Clinical severity classification

: based on observation of the peripheral cir-culation and on

auscultation of the lungs for congestion
Class I:
dry and warm

Class II:
wet and cold,
Class III:
cold and dry and
Class IV:
cold and wet).
Nohria A et al: JACC 2003;41:1797-1804.

 Clinical severity classification

dry: absence of signs of congestion, wet: elevated filling pressures,

warm: adequate systemic perfusion, cold: inadequate systemic perfusion
Nohria A et al: JACC 2003;41:1797-1804.

Clinical and pathophysiological

classification of acute heart failure
Congestion at rest

No

No

Yes

Warm & Dry

Warm & Wet

PCWP*
normal
CI normal

PCWP
elevated
CI normal

(compensated)

Low perfusion
at rest
Yes

Cold & Dry

Cold & Wet

PCWP
low/normal
CI decreased

PCWP
elevated
CI decreased

Normal SVR

Vasodilators,
diuretics

High SVR

More than 90% of patients hospitalized with heart failure have congestion (wet)
and show elevated PCWP1,2
References: 1. Stevenson LW. Tailored therapy to hemodynamic goals for advanced heart failure. Eur J Heart Fail. 1999;1:251-257.
Available at: http://www.sciencedirect.com/science/journal/13889842. 2. Fonarow GC. The treatment targets in acute decompensated

Hemodynamic subsets in acute heart

failure by cardiac index
Mor:10.1%

Cardiac index L/min/m 2

Mor:2.2%

Normal

Normal

2.2
2.0
1.5
1.0
0.5
0

high blood pressure

Pulmonary
edema

Mor:22.4%

normal blood pressure

Hypovolaemic
shock

Cardiogenic
shock

Mor:55.5%

reduced blood pressure

5

10

15

18

20 25

30

35

40

Pulmonary Wedge Pressure

Forrester et al: Am J Cardiol 1977; 39:137

Acute Heart Failure : Classification

The patient with AHF may present with one of several distinct clinical conditions:

Acute decompensated heart failure (de novo or as decompensation of CHF) : With mild signs and
symptoms of AHF and do not fulfil criteria for cardio-genic shock, pulmonary oedema or
hypertensive crisis.

Hypertensive acute heart failure: Signs and symptoms of HF + high BP + preserved LVF + chest
radiograph findings APO
.
Pulmonary oedema: Verified by chest X-ray, severe respiratory distress, or-thopnoea with SaO 2
<90%.

Cardiogenic shock: Reduced BP (SBP<90mmHg or drop of mean AP >30mmHg) and/or low urine
output (<0.5 ml/kg/h), with pulse rate >60 bpm with or without evidence of organ congestion.

High output failure: High CO + HR, pulmonary congestion, sometimes low BP (arrhythmias,
thyrotoxicosis, anaemia, Paget disease, iatrogenic etc)

Right heart failure: Low CO + increased jugular venous pressure + increased liver size + hypotension.

Underlying diseases and comorbidities in acute heart failure

Coronary artery disease
Valvular disease
Prosthetic valve thrombosis
Aortic dissection
AHF and hypertension
Renal failure
Pulmonary diseases and bronchoconstriction
Arrhythmias and AHF

Peri-operative

AHF

myocardial ischaemia)

(usually

due

to

Common Precipitating Factors

Medication non-adherence.
Dietary indiscretion.
Infection (pneumonia, UTI, etc.)
Renal failure.
Cardiotoxic/nephrotoxic
medication.
Uncontrolled hypertension
Cardiac Arrhythmias
Myocardial ishemia
Valvular disease

Pulmonary embolus
COPD
Anemia
Thyroid disorders
Nondihydropyridine CCB
Sodium retaining medications

Initial and Serial Evaluation of

the AHF Patient

Clinical Evaluation

Clinical Presentation
Volume Overload
Dyspnea/Fatigue
Rales/Wheezing
JVD/HJR/AJR
Pulmonary/Pitting Edema
Reduced oxygen saturation
S3 or S4
Electrolyte disturbance
Increased serum creatinine

Low Cardiac Output

Narrow Pulse Pressure
Altered Mental Status
Pre-renal azotemia
Cool extremities
Decreased urine output
Refractory to IV diuresis

The etiology of acute heart failure can vary

significantlly

Acute coronary
syndrom

Arterial hypertension,
diabetes mellitus

Primary dilated Toxic cardiomyopathy

cardiomyopathy
(cocaine, alchohol)

ADHERE registry: Treatment of

acute heart failure
ADHERE (Acute Decompensated HEart Failure National
REgistry)
Data from >100.000 patients
Database of demographic and clinical parameters of
hospitalized patients with decompensated heart failure

Clinical presentation of acute heart

failure in major clinical studies

Clinical presentations of acute heart failure

in EHFS II and ALARM-HF studies
EHFS II

ALARM-HF

Pulmonary oedema (16% vs 37%) and cardiogenic shock

(4% vs 12%) are significantly different between the two studies.

 Diagnosis
Epidemiology
Pathophysiology
Definition
Management
Summary of Guidelines
Recommended Reading

Diagnosic

ECG
CXR
ABG
Laboratory Tests
A small elevation
in cardiac
troponin may be
seen in patients
with AHF without
ACS.

Echo

Diagnostic approach to acute

heart failure

2014 AHA/ACC Guideline for the Management of Patients

Diagnosis
Low-Intermediate clinical suspicion of ADHF
BNP (A)

BNP > 500pg/ml

BNP 100-500pg/ml

ADHF more likely

Likely, but
consider other causes

BNP < 50-100pg/ml

ADHF less likely

Diagnosis: Cardiac Biomarkers

In patients with symptoms and signs of heart
failure:
Measure serum natriuretic peptides
Refer to have echocardiography and specialist
assessment within 2 weeks if
Previous MI
BNP > 400 pg/ml or
NTproBNP > 2000 pg/ml

If BNP < 100 pg/ml or NTproBNP < 400 pg/ml,

heart failure is unlikely in an untreated patient

Natriuretic
peptides
Negative
predictive value
There is no
consensus
regarding BNP or
NT-proBNP
reference values
in AHF.
Important
prognostic
information.

Cardiac Biomarkers
Troponin/BNP/CRP

Clinical Potential of BNP/NTproBNP

Extensively studied
A blood test for heart failure

Diagnosis-Raised in LVSD/AF/LVH/VHD/ACS
Screening for asymptomatic LVSD
Risk stratification & Prognosis in established HF
Therapy monitoring
Treatment of HF

Normal BNP makes LVSD very unlikely

NEGATIVE PREDICTIVE VALUE

Definitions
Epidemiology
Pathophysiology
Summary of Guidelines
Management
Summary of Guidelines
Recommended Reading

AHA/ACC Guideline
2014 AHA/ACC Guideline for the Management of Patients With Valvular
Heart Disease
A Report of the American College of Cardiology/American Heart Association
Task Force on Practice Guidelines
Rick A. Nishimura, MD, MACC, FAHA,

Applying guidelines in acute

heart failure: Facts or fancy?

EVIDENCE

ACCF/AHA Practice Guideline

40 pages

Canadian Cardiovascular Society

Consensus Recomendations

Australia/New Zealand
Heart Failure Guidelines

Treatment of acute heart failure

Balancing RISKS AND BENEFITS
for individual patients!

AHF

Definitions
Epidemiology
Pathophysiology
Management
(Nonpharmacological
treatment
.Summary of Guidelines
Recommended Reading

Various targets for therapies used in the

management of acute decompensated
heart failure.

Allen L A , and O'Connor C M CMAJ 2007;176:797-805

2007 by Canadian Medical Association

Noninvasive ventilation (NIV)

1. Bilevel positive airway pressure
(BiPAP) or
2. Continuous positive airway
pressure(CPAP).

Noninvasive PPV

Fig. 68-7

CPAP vs. Intubation

CPAP
Non-invasive
Easily discontinued
Easily adjusted
Use by EMT-B
Minimal complications
Does not require
sedation
Comfortable

Intubation
Invasive
Intubated stays intubated
Requires highly trained
personnel
Significant complications
Can require sedation or
RSI
Potential for infection

Ultrafiltration
RAPID-CHF Trial
40 patients
ADHF and Renal
Insufficiency (Cr >1.5)
Ultrafiltration had
significant increase in
fluid removal after 24
hours
4650 L vs 2838L

UNLOAD Trial
200 patients
Renal insufficiency was
not a criteria for inclusion
Standard care vs ultra
filtration
48 Hours 4.6 L vs 3.3L
90 Days fewer
rehospitalizations .22 vs .
46 and fewer unscheduled
clinic visits 21 vs 44

Option in the setting of failed diuretic

and vasodilator therapy

Cardiac and Ventricular Assist

Devices

Mechanical Circulatory Support

ECMO
VAD
IABP
Left Ventricular Assist Device
Right Ventricular Assist Device

Left Ventricular Assist Device

The LVAD assists left ventricular function by pumping

blood from left atrium to aorta

Right Ventricular Assist Device

The RVAD assists isolated right ventricular dysfunction by

pumping blood from right atrium to pulmonary artery

IABP

ECMO

Severe respiratory
failure Cardiac Failure
with inability to wean off
Bypass Bridge to
Cardiac Transplant

ECMO removes carbon dioxide

from and adds oxygen to venous
blood via an artificial membrane
lung

Acute Hert Failure and Operative

Mortality Prediction Score
Requirement for ventilator
support 4 points
Clinical picture of postcardiotomy shock 2 points
Use of temporary LVAD prior to
Heart-Mate insertion 2 points
Central venous pressure >16
mmHg 1 point
Prothrombin time >16 seconds
1 point

Scoring
0-5: Low risk
Mortality 8%
5-7: Intermediate Risk
Mortality 32%
8-10: High Risk
Mortality 49%

A brief
discussion of
the works of
this thing...

Questions

AFLEN

Triflusal

THE END

Thank you for your attention

New Strategies
for ANTIPLATELET

TRETMENT

Prof univ dr Ion C.Tintoiu

Ventricular Assist Device

.

Acute Heart Failure

Non-pharmachologic treatment
Balance between myocardial oxygen demand
and delivery
Temperature control
Mechanical circulatory support
Intraaortic balloon pump
Cardiopulmonary interaction; role of
mechanical ventilation

Ventricular Assist Device

Recent available specification
Centrifugal pump
Implantable pneumatic pulsatile Heartmate(Thermo
Cardiosystem)
Paracorporeal ABIOMED BVS 5000
pump(ABIOMED)
Paracorporeal pneumatic pulsatile Thoratec
VAD(Thoratec Laboratories)
Paracorporeal pulsatile pediatric VAD System
including Berlin Heart VAD(Mediport Kardiotechnik)
& MEDOS HIA-VAD System(BYTEC GmbH)
Jarvik 2000 System( Jarvik Research)

Intraaortic Balloon Pump

.

Extracorporeral Membrane Oxygenation

Advantages & disadvantages
Possibility of providing total cardiopulmonary support
and allowing for cardiac and pulmonary healing, but
needs for higher level of anticoagulation, leads to
bleeding, increased blood loss, blood product
requirement, multiple exploration, and potential
infection

Indications

Neonatal respiratory failure

Pediatric respiratory failure
Neonatal and pediatric cardiac failure
Adult cardiorespiratory failure

Mechanical Circulatory Support

Technical principles
In children, the most common form of VAD involves
use of centrifugal pump
Atrial pressure lines are neccessory to monitor for
adequate decompression and kept as close to zero as
possible to ensure ventricular decompression
All inotropes should be withheld if possible during the
recovery period
Serial stress echocardiography should be performed
every 1-3 days to document progression of recovery
Decannulation should be performed by gradually
weaning VAD support and be a team approach with
preparation of volume & catecholamine infusion ready.

Mechanical Assisted Circulation

Control of blood activation
Surface modifications
Inhibition of initial events
Platelet anesthesia
Contact phase inhibition
Complement inhibition
Monocyte inhibition

End-point inhibition
Antifibrinolytic drugs
Modulation of neutrophil-mediated injury

Surface Modifications
Methods of modification
Physical modification
Chemical modification by grafting
a hydrophilic component
Surface modification by inclusion
of bioactive components
Biomembrane mimicry
Cellular seeding and lining

Mechanical Circulatory Support

Complications
Hemorrhage
1. Local bleeding
2. Major intracranial hemorrhage
3. Coagulopathy and clot formation
Sepsis
Multisystem organ failure
Failure of myocardial recovery
Mortality

IABP in Pediatric Patients

Limitations
1. Inadequate hemodynamics due to increased
aortic elasticity
2. Rapid heart rate with small stroke volume
3. Technical difficulties related to insertion
4. Vascular occlusion of renal, mesenteric artery
& limb ischemia
5. Limited applications d/t small balloon

VAD for Pediatric Patients

Limitations of development
1 Size constraints
2 Differences in pathophysiology of failure
1)

Right ventricular failure

2)

Biventricular failure

3)

Pulmonary failure

Ventricular Assist Devices

Advantages
Providing good oxygen delivery to the tissue
Unloading the supported ventricle to allow time for
ventricular healing
Lower levels of anticoagulation than the ECMO

Disadvantages
Bleeding complication
Potential pulmonary dysfunction necessitating
conversion to ECMO
Potential for infection
Require a median sternotomy for direct access

Left Ventricular Assist Device

The LVAD assists left ventricular function by pumping

blood from left atrium to aorta

Right Ventricular Assist Device

The RVAD assists isolated right ventricular dysfunction by

pumping blood from right atrium to pulmonary artery

Berlin Heart VAD

Berlin Heart VAD is a paracorporeal air-driven pulsatile VAD

Jarvik 2000 System

Javik 2000 is an intraventricular axial flow impeller pump requiring

percutaneous electric power of possible implanted battery power

Biventricular Assist Device

Thoratec. BIVAD

Extracorporeral Membrane Oxygenation

Cardiopulmonary Support System

Initial and Serial Evaluation of

the AHF Patient

Clinical Evaluation

Initial and Serial Evaluation of

the AHF Patient

Diagnostic Tests

Initial and Serial Evaluation of

the AHF Patient

Noninvasive Cardiac
Imaging

Nonpharmacological
Interventions

Mechanical Circulatory
Support

Guideline for HF

Surgical/Percutaneous/
Transcatheter
Interventional
Treatments of AHF

Conclusions
Evidence-based guideline directed diagnosis, evaluation and
therapy should be the mainstay for all patients with HF.
Effective implementation of guideline-directed best quality
care reduces mortality, improves QOL and preserves health
care resources.
Ongoing research is needed to answer the remaining questions
including: prevention, nonpharmacological therapy of HF
including dietary adjustments, treatment of HFpEF,
management of hospitalized HF, effective reduction in HF
readmissions, more precise use of device-based therapy,
smaller MCS platforms and cell-based regenerative therapy.

Overview: Acute Heart Failure

New ESC guidelines
Diagnosis
Serum natriuretic peptides

Non-invasive ventilation
Inotropes
Nesiritide
Cardiac Devices

Objectives
Review the pathophysiology of ADHF.
Describe the clinical presentation of ADHF.
Apply effective therapeutic strategies using consensus
guidelines from the (HFSA) and the (ESC).
Examine the clinical evidence of milrinone and
niseritide in the treatment of ADHF.
Evaluate the appropriateness of treatment.

ADHF
Rapid onset of signs and symptoms secondary to abnormal cardiac
function due to systolic, diastolic dysfunction, abnormalities in
cardiac rhythm or to pre-load and after-load mismatch.
De novo or acute decompensation of CHF.
~50% of patients have a systolic blood pressure >140mmHg.
~46% of patients have a preserved (LVEF).
Patients often present with multiple co-morbidities.
Killip Classification.
Forrester Classification.
Clinical Severity Classification.

Pathophysiology
LV dysfunction:
Accumulation of fluid.
Decrease in CO
Hypoperfusion.
Reciprocal Activation of (RAAS)
Na, water retention.
AGII
ET1 + Vasopressin.
Reflex activation of SNS: Epi, NE.

Acute heart failure

AHF: The rapid onset of symptoms and signs secondary to
abnormal
cardiac function.
(reduced CO, tissue hypoperfusion + congestion, increase in PCWP)
1.
2.

3.

With or without previous cardiac disease.

The cardiac dysfunction can be related:
a) to systolic or diastolic dysfunction
b) to abnormalities in cardiac rhythm
c) to preload and afterload mismatch
Often life threatening and requires urgent treatment.

The Task Force on Acute Heart Failure of the European Society of

Cardiology

Hemodynamic subsets in acute heart

failure
Mor:10.1%

Cardiac index L/min/m 2

Mor:2.2%

Normal

Normal

2.2
2.0
1.5
1.0
0.5
0

high blood pressure

Pulmonary
edema

Mor:22.4%

normal blood pressure

Hypovolaemic
shock

Cardiogenic
shock

Mor:55.5%

reduced blood pressure

5

10

15

18

20 25

30

35

40

Pulmonary Wedge Pressure

Forrester et al: Am J Cardiol 1977; 39:137

Acute Heart Failure :

Other Classifications
In AHF after AMI, best applied to acute denovo heart failure:

The Killip classification :

based on clinical signs and chest X-ray findings (Stage I: No heart failure, Stage II: Heart
failure, Stage III: Severe heart failure and Stage IV: Cardiogenic shock).
The Forrester classification
: based on clinical signs and haemodynamic cha-racteristics.

In a cardiomyopathy service, best applied to chronic decompensated heart failure:

Clinical severity classification :

based on observation of the peripheral cir-culation and on auscultation of the lungs for
congestion
(Class I: dry and warm, Class II: wet and cold, Class III: cold and dry and Class IV: cold and
wet).
Nohria A et al: JACC 2003;41:1797-1804.

Acute Heart Failure : Classification

The patient with AHF may present with one of several distinct clinical conditions:

Acute decompensated heart failure (de novo or as decompensation of CHF) : With

mild signs and symptoms of AHF and do not fulfil criteria for cardio-genic shock,
pulmonary oedema or hypertensive crisis.
Hypertensive acute heart failure: Signs and symptoms of HF + high BP + preserved
LVF + chest radiograph findings APO.
Pulmonary oedema: Verified by chest X-ray, severe respiratory distress, or-thopnoea
with SaO2 <90%.
Cardiogenic shock: Reduced BP (SBP<90mmHg or drop of mean AP >30mmHg)
and/or low urine output (<0.5 ml/kg/h), with pulse rate >60 bpm with or without
evidence of organ congestion.
High output failure: High CO + HR, pulmonary congestion, sometimes low BP
(arrhythmias, thyrotoxicosis, anaemia, Paget disease, iatrogenic etc)
Right heart failure: Low CO + increased jugular venous pressure + increased liver
size + hypotension.

The Task Force on Acute Heart Failure of the European Society of Cardiology

Acute Heart Failure : Classification

HR

SBP

CI

PCWP

Congestion
Killip/
Forrester

Diuresis

Hypoperfusion

End organ
hypoperfusion

+/-

Low
Normal
/
High

Low
normal /
High

Mild
elevation

K II / F II

+/-

II Acute heart
failure with
hypertension/
hypertensive crisis

Usually
increased

High

+/-

>18

K II- IV/ FII-III

+/-

+/-

+, with CNS
symptoms

III Acute heart

failure with
pulmonary oedema

Low
normal

Low

Eleva
ted

KIII/ FII

+/-

Cardiogenic
shock*:
IVa. Low output
syndrome

Low
normal

Low, <2.2

>16

K III-IV /
F I-III

low

IVb Cardiogenic
shock

>90

<90

<1.8

>18

K IV/ F IV

Very low

++

+/-

+/-

KII/FI-II

Usually
low

Low

Low

Low

FI

+/-

+/-, acute
onset

+/-

I. Acute
decompensated
congestive heart
failure*

V. High output
failure
VI. Right sided
acute heart failure

Underlying diseases and comorbidities in acute heart failure

Coronary artery disease
Valvular disease
Prosthetic valve thrombosis
Aortic dissection
AHF and hypertension
Renal failure
Pulmonary diseases and bronchoconstriction
Arrhythmias and AHF

Peri-operative

AHF

myocardial ischaemia)

(usually

due

to

Goals of treatment of the patient

with acute heart failure
Clinical

symptoms (dyspnea and/or fatigue)

clinical signs
body weight
diuresis
oxygenation

Laboratory examinations

BUN and/or creatinine

serum electrolyte normalisation
plasma BNP
blood glucose normalisation

Haemodynamic
pulmonary wedge pressure to < 18 mm Hg
cardiac output and/or stroke volume

The Task Force on Acute Heart Failure of the European Society of Cardiology

Goals of treatment of the patient

with acute heart failure
Outcome
length of stay in the intensive care unit
duration of hospitalization
time to hospital re-admission
mortality
Tolerability
Low withdrawal rate
Low incidence of adverse effects

The Task Force on Acute Heart Failure of the European Society of Cardiology

Ventricular function

Acute Exacerbations May Contribute to

the Progression of the Disease
With each event,
hemodynamic alterations
contribute to progressive
ventricular dysfunction.

Acute event

Time
Gheorghiade M, Fonarow G, Filippatos G et al. Am J Cardiology 2005

Killip Classification
Stage I: No clinical signs of decompensation.
Stage II: Heart failure. Rales, S3, PVH.
Stage III: Severe heart failure. Pulmonary edema with
rales throughout the lung fields.
Stage IV: Cardiogenic Shock: Hypotension, peripheral
vasoconstriction, oliguria, cyanosis and diaphoresis.

Forrester Classification
Cardiac Index
(L/min/m2)
5
4

18 mmHg

Subset I
(Normal)
Warm and Dry

Subset II
(Congestion)
Warm and Wet

Subset III
(Hypoperfusion)
Cold and Dry

Subset IV
(Congestion and
hypoperfusion)
Cold and Wet

3
2.2L/min/m2

2
1

10

20

Pulmonary Capillary Wedge Pressure (mmHg)

30

Nohria A et al. JAMA.2002:287; 628-40

Common Precipitating Factors

Medication non-adherence.
Dietary indiscretion.
Infection (pneumonia, UTI, etc.)
Renal failure.
Cardiotoxic/nephrotoxic
medication.
Uncontrolled hypertension
Cardiac Arrhythmias
Myocardial ishemia
Valvular disease

Pulmonary embolus
COPD
Anemia
Thyroid disorders
Nondihydropyridine CCB
Sodium retaining medications

Clinical Presentation
Volume Overload
Dyspnea/Fatigue
Rales/Wheezing
JVD/HJR/AJR
Pulmonary/Pitting Edema
Reduced oxygen saturation
S3 or S4
Electrolyte disturbance
Increased serum creatinine

Low Cardiac Output

Narrow Pulse Pressure
Altered Mental Status
Pre-renal azotemia
Cool extremities
Decreased urine output
Refractory to IV diuresis

Differential Diagnosis
Pneumonia
Reactive airway disease
Pulmonary embolus

Diagnosis
Diagnosis of ADHF should be primarily
based on signs and symptoms. (C)

Diagnosis
Low-Intermediate clinical suspicion of ADHF
BNP (A)

BNP > 500pg/ml

BNP 100-500pg/ml

ADHF more likely

Likely, but
consider other causes

BNP < 50-100pg/ml

ADHF less likely

Predictors of Mortality
BUN > 43 mg/dl
SBP < 115 mmHg
sCr >2.75 mg/dl

Highest risk
of mortality

Fonarow GC et al. JAMA. 2005;293:572-80

Diagnosis: Cardiac Biomarkers

In patients with symptoms and signs of heart
failure:
Measure serum natriuretic peptides
Refer to have echocardiography and specialist
assessment within 2 weeks if
Previous MI
BNP > 400 pg/ml or
NTproBNP > 2000 pg/ml

If BNP < 100 pg/ml or NTproBNP < 400 pg/ml,

heart failure is unlikely in an untreated patient

Natriuretic
peptides
Negative
predictive value
There is no
consensus
regarding BNP or
NT-proBNP
reference values
in AHF.
Important
prognostic
information.

Cardiac Biomarkers
Troponin/BNP/CRP

New Classification of MI-Type

2?
Secondary to
spasm,
embolism, anaemia,
arrhythmia, BP
changes
Type 1

Type 2

Troponinitis

Acute MI

Type 3

Type 4

Type 4a

Type 5

Type 4b

Clinical Potential of BNP/NTproBNP

Extensively studied
A blood test for heart failure

Diagnosis-Raised in LVSD/AF/LVH/VHD/ACS
Screening for asymptomatic LVSD
Risk stratification & Prognosis in established HF
Therapy monitoring
Treatment of HF

Normal BNP makes LVSD very unlikely

NEGATIVE PREDICTIVE VALUE

Overview: Acute Heart Failure

New ESC guidelines
Diagnosis
serum natriuretic peptides

Non-invasive ventilation
Inotropes
Nesiritide
Cardiac Devices

Acute Cardiogenic Pulmonary Oedema

Common
15-20,000 hospital
admissions per annum in
UK

Deadly
15-20% in-hospital
mortality

Costly
6.5 million hospital days
per annum in USA

Initial Treatment
The evidence in
favour of morphine
use for AHF is
limited.
Multiple agents are used
to manage AHF, but
there is a paucity of
clinical trials data and
their use is largely
empiric.
Most agents improve
haemodynamics but no
agent has been shown
to reduce mortality.

Non-invasive Ventilation In Acute Cardiogenic

Pulmonary Oedema

When the household vacuum cleaner is employed,

the machine should be run for some minutes first of
all to get rid of dust
Poulton EP, Oxon DM: Left-sided heart failure with
pulmonary oedema: Its treatment with the "pulmonary
plus pressure machine." Lancet (1936);231:981-983.

Physiological Improvement with CPAP in Patients

with ACPO

Reduced acidosis, respiratory rate and heart rate

Kelly et al. Eur Heart J 2002;

Mortality Benefit of CPAP/NIPPV in Patients with

ACPO
Mortality reduced
from 22% to 11%
RR 0.53
(95% CI 0.35-0.81)
(Individual Group
Sizes small)
However, in 3CPO,
a large RCT........

Masip et al. JAMA 2005;29

3CPO

Trial summary

Background
Aims

Clinical effectiveness of noninvasive ventilation

Comparative effectiveness of
CPAP and NIPPV
Safety of non-invasive ventilation

Hypothesis:

Non-invasive ventilation reduces

mortality

Intervention

Randomised (1:1:1)

Standard oxygen
therapy (by facial mask)
CPAP (5 cmH2O up
titrated to a maximum
of 15 cmH2O)
NIPPV (8/4 cmH2O up
titrated to a maximum
of 20/10 cmH2O)
Inhaled oxygen of 60%
Attending physicians were
encouraged to use
vasodilator (nitrate) and
diuretic therapy
Opiate therapy was
administered at the
discretion of the treating
physician

3CPO

Outcome: Any NIV v Standard

Mortality
Standard
Therapy

NonInvasive
Ventilation

Odds Ratio

95%
Confidence
Intervals

P Value

7-Day

9.8%

9.5%

0.97

0.63 to 1.48

0.869

30-Day

16.7%

15.4%

0.93

0.65 to 1.32

0.685

Active Trial 1069 patients ~ 350 per arm

Baseline Characteristics matched
Baseline Medications matched

3CPO

Outcome: Hospital stay

Standard

CPAP

NIPPV

P-value

Admitted to intensive
Care

8.8%

9.1%

6.6%

0.411

Admitted to highdependency Care

7.7%

10.3%

10.9%

0.301

Admitted to coronary
Care

38.1%

43.7%

40.9%

0.337

9 (5-16)

9 (5-16)

0.313

Median length of hospital 8 (5-13)

stay in days ( IQR)

No significant differences (P>0.05)

3CPO
CONCLUSIONS
In patients with acute cardiogenic pulmonary
oedema non-invasive ventilation (1069 patients)
Produces more rapid resolution of metabolic abnormalities
and respiratory distress
Has no major effect on 7-day or 30-day mortality
Is beneficial irrespective of the mode (CPAP or NIPPV) of
delivery

Overview: Acute Heart Failure

New ESC guidelines
Diagnosis
serum natriuretic peptides

Non-invasive ventilation
Inotropes
Nesiritide
Cardiac Devices

Treatment related to BP

Respiratory support, Furosemide (infusion)

IV Dobutamine plus low dose IV GTN
IABP

Other treatment options

Vasopressin antagonists
Unproven
Levosimendan is a calcium
sensitiser that improves
cardiac contractility
Exerts significant
vasodilatation mediated
through ATP-sensitive
potassium channels

Levosimendan infusion
increases cardiac output
and stroke volume and
reduces pulmonary wedge
pressure, systemic vascular
resistance, and pulmonary
vascular resistance.
Vasopressors
(norepinephrine) are not
recommended as first-line
agents

Overview: Acute Heart Failure

New ESC guidelines
Diagnosis
serum natriuretic peptides

Non-invasive ventilation
Inotropes
Nesiritide
Cardiac Devices

Causes of death in heart failure

NYHA II

NYHA III

12%
24%
64%

Pump failure
Other
Sudden death

26%

NYHA IV
33%

59%
15%

56%

11%

I
No Limitation
II
SOB on severe
exertion
III
SOB on mild
exertion

Pre-implant counselling
How do you want to die?
Heart failure death

Sudden death

Device X Rays
ICD Lead

BiV LV Lead position

ICD Myths
Myths
ICDs prevent syncope
Contacts can be electrocuted by
ICD discharge
Not safe to use mobile phone,
mircowave, playstation etc.
Will stop you dying from VF

Diathermy kills patients

& devices
PPM may inhibit (pulse
oximetry)
ICD will detect as VF
(reprogram)

Consequences of tachycardia therapy

VT Storm

Inappropriate shocks

End of life issues: NECVN

Ventricular arrhythmias and/or poor LV function is an ICD indicated ?

Temporarily disabled with a ring magnet

The Future?

Intrathoracic Impedance: Concept

The Reality

Drier
lungs
means
the
intrathor

Less
Fluid

Wetter
lungs
means
the
intrathor

More
Fluid

Epidemiology
~ 5 million
Dx in
US

~550 000 new

cases/yr
~ 1 million
hospitalizations/ yr
Mortality is approx. 50% at 5 years
Economic Costs approx. 29.6 billion $
(direct and indirect costs)
Heart disease and stroke statistics- 2006 Update, American Heart Association

Objectives
Review the pathophysiology of ADHF.
Describe the clinical presentation of ADHF.
Apply effective therapeutic strategies using consensus
guidelines from the (HFSA) and the (ESC).
Examine the clinical evidence of milrinone and
niseritide in the treatment of ADHF.
Evaluate the appropriateness of treatment.

ADHF
Rapid onset of signs and symptoms secondary to abnormal cardiac
function due to systolic, diastolic dysfunction, abnormalities in
cardiac rhythm or to pre-load and after-load mismatch.
De novo or acute decompensation of CHF.
~50% of patients have a systolic blood pressure >140mmHg.
~46% of patients have a preserved (LVEF).
Patients often present with multiple co-morbidities.
Killip Classification.
Forrester Classification.
Clinical Severity Classification.

Pathophysiology
LV dysfunction:
Accumulation of fluid.
Decrease in CO
Hypoperfusion.
Reciprocal Activation of (RAAS)
Na, water retention.
AGII
ET1 + Vasopressin.
Reflex activation of SNS: Epi, NE.

Killip Classification
Stage I: No clinical signs of decompensation.
Stage II: Heart failure. Rales, S3, PVH.
Stage III: Severe heart failure. Pulmonary edema with
rales throughout the lung fields.
Stage IV: Cardiogenic Shock: Hypotension, peripheral
vasoconstriction, oliguria, cyanosis and diaphoresis.

Forrester Classification
Cardiac Index
(L/min/m2)
5
Subset I
4

18 mmHg

(Normal)
Warm and Dry

Subset II
(Congestion)
Warm and Wet

3
2.2L/min/m2

2
1

Subset III
(Hypoperfusion)
Cold and Dry
10

Subset IV
(Congestion and
hypoperfusion)
Cold and Wet
20

Pulmonary Capillary Wedge Pressure (mmHg)

30

Nohria A et al. JAMA.2002:287; 628-40

Common Precipitating Factors

Medication non-adherence.
Dietary indiscretion.
Infection (pneumonia, UTI, etc.)
Renal failure.
Cardiotoxic/nephrotoxic
medication.
Uncontrolled hypertension
Cardiac Arrhythmias
Myocardial ishemia
Valvular disease

Pulmonary embolus
COPD
Anemia
Thyroid disorders
Nondihydropyridine CCB
Sodium retaining medications

Clinical Presentation
Volume Overload
Dyspnea/Fatigue
Rales/Wheezing
JVD/HJR/AJR
Pulmonary/Pitting Edema
Reduced oxygen saturation
S3 or S4
Electrolyte disturbance
Increased serum creatinine

Low Cardiac Output

Narrow Pulse Pressure
Altered Mental Status
Pre-renal azotemia
Cool extremities
Decreased urine output
Refractory to IV diuresis

Differential Diagnosis
Pneumonia
Reactive airway disease
Pulmonary embolus

Diagnosis
Diagnosis of ADHF should be primarily
based on signs and symptoms. (C)

Diagnosis
Low-Intermediate clinical suspicion of ADHF
BNP (A)

BNP > 500pg/ml

BNP 100-500pg/ml

ADHF more likely

Likely, but
consider other causes

BNP < 50-100pg/ml

ADHF less likely

Predictors of Mortality
BUN > 43 mg/dl
SBP < 115 mmHg
sCr >2.75 mg/dl

Highest risk
of mortality

Fonarow GC et al. JAMA. 2005;293:572-80

Goals of Therapy
Improve symptoms and signs of congestion and/or
hypoperfusion.
Reverse hemodynamic abnormalities.
Identify the etiology.
Minimize side effects.
Optimize therapy.
Length of stay, mortality, time to hospital
readmission.*
Educate patients on medications and self assessment
of HF.

Treatment Strategy

Establish a Diagnosis
Oxygen and Ventilatory Assistance
Symptom Relief
Anticoagulation
Hemodynamic Support:

Diuresis/Fluids
Vasodilators
Inotropes
Vasopressors

Assess Patient Response

Anti-infectives
Glucose Control

The Principle
Diuretics

Reduce Fluid Overload

Reduced Preload: (E-DVf), PCWP

Inotropes

Increase Contractility
Increase CO, EF, Perfusion

Vasodilators

Reduce Preload
Reduce Afterload

Assess Signs/Symptoms/Determine
Hemodynamic Status
EC Interventions:
Cardiac panel: (CBC w/diff & platelets, SMA-7
CK-MB, Glucose), TSH,
Pox, ECG, BNP, X-ray
Abnormal
Evaluate cardiac function by 2DE
Characterize type and severity
Is patient hypoxic?
Yes
No but difficult breathing
Oxygen C
CPAP
NIPPV

Normal
Consider
alternative diagnosis
Does Patient presents with
Distress or pain ?

yes
Morphine 3 mg IVPB IIbB
Does patient present with ischemic chest
pain resistant to opiates or tachycardia?
Metoprolol 5 mg IV* IIbC

Volume Overloaded
(A) Moderate Volume Overload
IV Diuretics
Furosmide 20-40 mg
Bumetanide 0.5-1.0 mg
Torasemide 10-20 mg
IB/B
Inadequate Response
< 250-500 ml within 2 hours
Na/fluid restriction
Add HCTZ 25-50 mg bid, or
Metolazone 2.5-10 mg qd, or
Spironolactone 25-50 mg qd
IIbC/C

Consider Dopamine <2-3 ug/kg/min IIbC

Ultrafiltration or Hemodialysis C
Consider Severe Volume Overload (B)
Or Low Cardiac Output (C)
Refractory to loop + thiazides

(B) Severe Volume Overload

SBP>90 mmHg
IV Diuretics +/- IV Vasodilators
Furosmide 40-100 mg IV then 5-40 mg/h inf.
Bumetanide 1-4 mg
Torasemide 20-100 mg
PLUS
Nitroglycerin 5-10 ug/min inf.*
Class IIbC/C

(C) Low Cardiac Output

SBP >100 mmHg

SBP 85-100 mmHg

Vasodilator
(NTG, Nitroprusside)C

SBP < 85 mmHg

On a B-blocker chronically?

Volume repletion
Inotrope IIaC/C
Yes/No
No or D/C
And/or
Dobutamine IIaCC
Consider D/C or reducing
Dopamine
2-3 ug/kg/min inf.
dose if sign of excessive
>5ug/kg/min
-20ug/kg/min inf.
dose are suspected

Milrinone 25-75ug/kgIVPB over10-20min Hypoperfusion resolving?

Then 0.37-0.75ug/kg/min inf. IIbC/IIaC*C
yes

No

Tapper off dobutamine

by steps of 2 ug/kg/min qod
+optimize tx with hydralazine and/or ACE-I

(D)

(D) Unresolved hypoperfusion

Use of invasive
hemodynamic monitoring C

Transient use of Vasopressor therapy

Epinephrine
0.05-0.5 ug/kg/min inf. Norepinephrine 0.2-1ug/kg/min
+/- dobutamine
0.05-0.5 ug/kg/min inf.

Monitoring Parameters

Oxygen Saturation
CBC
BP
ECG
BNP
Signs:
Edema, Rales, Ascites, Hepatomegaly, JVD
Symptoms:
Orthopnea, PND, Dyspnea, Fatigue, Cough
Negative/positive balance
Electrolytes
Urinalysis
BUN/Scr
ABG

(OPTIME-CHF)
Outcomes of a Prospective Trial of
Intravenous Milrinone for Exacerbations of
Chronic Heart Failure
JAMA, March 27 2002: 287(12);1541-1547

Objective: To prospectively test whether a strategy that includes shortterm

use of milrinone in addition to standard therapy can improve clinical outcomes
of patients hospitalized with an exacerbation of chronic heart failure.

Study Design
Prospective randomized double-blind placebocontrolled trial.
ITTA.
Similar baseline characteristics.
Randomization to a 48 hour infusion of either
milrinone (n = 477) or placebo ( 472).
Milrinone treatment arm: Started with an initial
infusion of 0.5ug/kg/min for 48hrs. (Rate adjusted to
0.375 ug/kg/min)

Outcome Measures
Primary Efficacy Outcome:
The total number of days hospitalized for cardiovascular causes or
days decreased within the 60 days after randomization.

Secondary endpoints:

Failed therapy because of adverse events.

Failed therapy because of worsening heart failure.
Proportion of patients achieving target doses of ACE-I therapy.
Time to achieve target ACE-I dose.
Symptom improvement in HF score.

Patient Selection
Inclusion Criteria
18 yoa
Demonstrated LVEF < 40%

Exclusion Criteria
-If physician judged that
inotropic therapy was
essential.
-Active myocardial ischemia
within past 3 months.
-Atrial fibrillation with poor
ventricular rate control.
-Sustained VT/Vf.

Results
Treatment with milrinone did not reduce the primary
endpoint of days hospitalized for cardiovascular causes
within 60 days compared with placebo.

Results (cont)
Placebo
(n=472)
Treatment failure cause at 48 hours:
Adverse event
Events during hospitalization:
MI
New atrial fibrillation/flutter
Ventricular tachycardia/fibrillation
Sustained hypotension

Milrinone
(n = 477)

P value

2.1%

12.6%

<0.001

0.4%
1.5%
1.5%
3.2%

1.5%
4.6%
3.4%
10.7%

<0.18
<0.04
<0.06
<0.001

Limitations
Study did not directly address patients with
acutely decompensated chronic heart failure for
whom inotropic therapy is essential.
Non-formal therapeutic protocol.*
Confounding variables.

Conclusions
Results do not support the routine use of
milrinone in patients hospitalized with an
exacerbation of chronic heart failure.

(VMAC)
Intravenous Nesiritide vs Nitroglycerin
for Treatment of Decompensated
Congestive Heart Failure

Objective: To compare the efficacy and safety of

intravenous nesiritide, intravenous nitroglycerin
and placebo.

Study Design
Randomized double-blind, double dummy trial.
Patients were stratified to catheterized (n=246) and
non-catheterized (n= 243)
Patients were then randomized to fixed dose nesiritide,
adjustable dose niseritide, nitroglycerin or placbo for
the first 3 hours.
After 3 hours patients were in the double dummy
design of nesiritide and nitroglycerin treatment arms.

Outcome Measures
Primary Endpoint: Change in PCWP and patients
self-evaluation of dyspnea from baseline at 3hours.
Secondary Endpoints:

Onset of effect on PCWP

Effect on PCWP 24 hrs after the start of study drug
Self-assessed dyspnea and global clinical status
Overall safety profile.

Inclusion
Inclusion Criteria
Dyspnea at rest
Cardiac etiology of dyspnea

Exclusion Criteria
SBP<90
Volume depletion
CI to IV vasodilators
Mechanical ventillation
Survival less than 35 days

Results
Reduction in PCWP was greater in the
nesiritide group with the first measurement.
Beyond 24hr the difference in PCWP between
nesiritide and nitroglycerin was insignificant.
Improvement in dyspnea and global clinical
status scores in the nesiritide and nitroglycerin
were not significantly different at any time.
HA was more common in the Nitroglycerin
group.

Limitations
Heterogenous patient population*
Therapeutic protocol.
Assessment of mortality/morbidity

Conclusion
When added to standard care in hospitalized
patients with ADHF, nesiritied improves
hemodynamic function and some selfreported symptoms more effectively than
intravenous nitroglycerin.

CC: Weakness and Shortness of Breath.

4/06/07 (ER)
HPI:
BH is a 95 year-old female with a known history of
CHF, HTN, anxiety. Patient presents with altered
mentation along with swelling in the legs and arms.
PMH:
HTN, CVA, chronic atrial fibrillation, anxiety.

Allergies: PCN (rash)

SH: Lives at home, has a 24 hour caregiver.
Medications at Home: Atenolol 25 mg qd, pantoprazole 40mg qd,
ASA 81 mg qd, lorazepam 1 mg qhs, clopidogrel 75 mg qd,
acetaminophen 500 mg qid prn, ciprofloxacin 500mg bid.

Physical assessment: 3+ edema from waist down.

VS: H=411 W=50.0kg T= 36oC, P= 96, RR=18,BP=114/86
HEENT: conjunctivae and lids have no pallor and no
jaundice. Pupils equal, round and reactive to light and
accomodation. Ears, nose and throat normal.

Lungs: bilateral basilar crackles.

CV: heart rhythm irregular.
Abd: soft. no n/v/d, no hepatosplenomegaly.
Neuro: lethargic. GCS:14.
Labs:
Na 139
WBC 10.5 Scr 1.8 BNP 1343
K 4.1
HGB 9.6 BUN 30 AG 9
Cl 108
HCT 48
Plt 296 CK 171 MB 6.4
X-Ray: small left effusion, atelectasis, no pneumothorax.
EKG: atrial fibrillation w ventricular response, with T
wave
inversions.

Physicians assessment/plan:
1. Congestive Heart Failure: Patient will receive IV
diuretics and monitor for electrolytes.
2. UTI: Continue Cipro until the completion of the course.
3. Abnormal cardiac enzymes: Represent myocardial
injury. Cardiology consulted.
4. Acute Renal insufficiency: Monitor creatinine, diuresis
and BP.

AHA/ACC Guideline
2014 AHA/ACC Guideline for the Management of Patients With Valvular
Heart Disease
A Report of the American College of Cardiology/American Heart Association
Task Force on Practice Guidelines
Rick A. Nishimura, MD, MACC, FAHA,

Evaluation and Management of CAD in Patients Undergoing Valve Surgery CABG indicates
coronary artery bypass graft; CAD, coronary artery disease; CT, computed tomography; IE,
infective endocarditis; LV, left ventricular; and PCI, percutaneous coronary intervention.

Nishimura R A et al. Circulation. 2014;129:e521-e643

Copyright American Heart Association, Inc. All rights reserved.

Diagnosis and Treatment of IE. *Early surgery defined as during initial hospitalization before
completion of a full therapeutic course of antibiotics.

Nishimura R A et al. Circulation. 2014;129:e521-e643

Copyright American Heart Association, Inc. All rights reserved.

The definition of acute heart

failure has not been firmly
established ().

It is recognized when symptoms of

heart failudevelop rapidly within
hours and
days in patients without prior
evidence of cardiac
decompensation

Drug

Usual
Dose

Vaso
dilati
on

Vasocon
strixn

Inotro
pic

Chronot
ropic

HR

MAP

PAP

PWP

CVP

SVR

SV

CO

Epinephrine
(Adrenaline)

0.01-0.1
g/kg/min
0.1-0.5
g/kg/min
(1-4
g/min)

+++

++

++

+++

++

+++

++

++

+++

++

++

Norepinephrine
(Levophed)

0.03-1.5
g/kg/min
(2-80
g/min)

++++

++

++++

+*

O/

Dopamine
(Dobutrex)

1-3
g/kg/min
3-8
g/kg/min
8-20
g/kg/min

O/

O/

O/

O/

O/

O/

++

++

++

++

+++

++

+++

++

++

Drug

Usual Dose

Vas
odi
lati
on

Vasoc
onstri
xn

Inotr
opic

Chro
notro
pic

H
R

MA
P

PAP

PW
P

CV
P

SV
R

S
V

C
O

Dobutami
ne
(Dobutre
x)

2-30
g/kg/min

+++

++

++

+++

O/

O/

O/

O/

O/

O/

Milrinone
(Primacor
)

LD 50 g/kg
over 10 min.,
then 0.3750.75
g/kg/min

++
+

+++

O/

O/

Gilman AG, Rall TW., et al. Goodman and Gilmans The Pharmacological Basis of Therapeutics. 8th ed. 1993.
Marino P. The ICU Book. 2nd ed. 1998. Young L., Koda-Kimble M. Applied Therapeutics. 6th ed. 1995.
Kirby R., Taylor R., et. al. Handbook of Critical Care. 2nd ed. 1997.
Darovic G., Franklin C. Handbook of Hemodynamic Monitoring. 1999.

Nuove prospettive nel trattamento

dello scompenso acuto

Michele Emdin,
Fondazione Gabriele Monasterio, Pisa

Congresso regionale ANMCO Toscana,

Viareggio, 7 OTTOBRE 2011

Acute Heart Failure Syndrome(s)

Acute heart failure (AHF) is defined as a rapid onset

or change in the signs and symptoms of HF, resulting
in the need for urgent therapy.

Symptoms are primarily the result of severe

pulmonary congestion due to elevated left ventricular
(LV) filling pressures (with or without low cardiac
output).

AHFS can occur in patients with preserved or reduced

ejection fraction (EF).

Concurrent cardiovascular conditions such as coronary

heart disease (CHD), hypertension, valvular heart
disease, atrial arrhythmias, and/or noncardiac
conditions (including renal dysfunction, diabetes,
anemia) are often present and may precipitate or
contribute to the pathophysiology of this syndrome

AHFS: NOT VERIFIED

EBM in AHFS?

The first randomized placebo-controlled AHFS trials

were published as late as 2002.
Cuffe MS, et al. for the Outcomes of a Prospective Trial of Intravenous Milrinone for Exacerbations of Chronic Heart Failure (OPTIME-CHF)
Investigators. Effects of short-term, intravenous milrinone on acute exacerbation of chronic heart failure: a randomized controlled trial. JAMA. 2002;
287: 15411547.

Publication Committee for the VMAC Investigators. Intravenous nesiritide vs nitroglycerin for treatment of decompensated congestive heart failure: a
randomized controlled trial. JAMA. 2002; 287: 15311540

None of the placebo-controlled AHFS studies conducted

to date has shown either a consistent improvement of inhospital or postdischarge survival or a decrease in
readmissions.

AHFS Goals of treatment

Emergency treatment phase

Improve symptoms
Restore oxygenation
Improve organ perfusion and haemodynamics
Limit cardiac/renal damage
Minimize ICU length of stay

In-hospital management phase

Stabilize patient and optimize treatment strategy

Initiate appropriate (life-saving) pharmacological therapy
Consider device therapy in appropriate patients
Minimize hospital length of stay
Discharge planning phase
Plan follow-up strategy
Educate and initiate appropriate lifestyle adjustments
Provide adequate secondary prophylaxis
Prevent early readmission
Improve quality of life and survival

AHFS: which appropriate targets

of therapy ?
Traditionally, reduction in pulmonary capillary
wedge pressure (PCWP) and/or increase in
cardiac output.
However, other therapeutic targets may include
blood pressure control, myocardial protection,
neurohormonal modulation, and preservation
of renal function.

Treatment of AHFS Patients

The emergency treatment phase

Patient Selection and Treatment

Congestion at Rest
No
No

Low
Perfusion
at Rest Yes

Warm & Dry

PCWP normal
CI normal
(compensated)

Cold & Dry

PCWP low/normal
CI decreased

Yes

Warm & Wet

PCWP elevated
CI normal
Cold & Wet
PCWP elevated
CI decreased
Normal
SVR

Inotropic Drugs
Dobutamine
Milrinone
Calcium Sensitizers
Stevenson LW. Eur J Heart Fail. 1999;1:251.

High
SVR

Natriuretic
Peptide
Nesiritide
or
Vasodilators
Nitroprusside
Nitroglycerin

Recommended approach to the use of inotropic support in

patients hospitalized with acute HF exacerbation

Goldhaber, J. I. et al. Circulation 2010;121:1655-1660

Copyright 2010 American Heart Association

Adverse Drug Effects

Non-Potassium-Sparing Diuretics
Intravenous loop diuretics may improve symptoms and fluid loss initially but also
may contribute to renal function decline. This may be related not only to
intravascular volume depletion but also to further neurohormonal activation
resulting in a vasomotor nephropathy.
Intravenous loop diuretics may be associated with worse outcomes in AHFS patients.

Inotropic Therapy
Intravenous inotropes increase myocardial oxygen consumption, causing myocardial
damage in the setting of hibernating myocardium. Use of inotropes has consistently
been associated with increased mortality.

Vasodilators
Excessive vasodilatation in AHFS may lead to blood pressure decrease, potentially
exacerbating myocardial ischemia and renal hypoperfusion.

AHFS: which appropriate targets

of therapy ?
Perspectives
Managing fluids,
Preserving renal function

AHFS: which appropriate targets

of therapy ?

Contractility
Diastole

AHFS: Non farmachological

therapy

Vasomotion

AHFS where are we? Where are we going?

AHFS is a complex condition with substantial morbidity and mortality and
enormous utilization of health resources and cost.
There are numerous challenges in caring for this population.
Uniform AHFS classification is currently lacking, and management
strategies vary markedly.
There is a general consensus that to reduce mortality, morbidity, and the
economic burden of AHFS, systematic research efforts on clinical application
and translation of promising basic science results are needed.
Pathophysiologically based interventions (eg, cardiorenal syndrome) may be
particularly appealing.
A special focus should be on choice of appropriate management strategies,
including minimizing the use of drugs with adverse effects and development
and validation of known prognostic markers to guide AHFS interventions.

CONCLUSION
...of note, every large published clinical trial
conducted in patients with AHFs has been negative
in terms of efficacy, safety, or both.
However, most international multicenter clinical
trials completed to date were conducted on fairly
undifferentiated populations of patients with AHFs.
.homogeneous pathophysiological disease states
within the heterogeneity of aHFs is of paramount
importance to clinical trial design and aHFs therapy.
Future trials conducted in aHFs must abandon
the one-sizefits- all approach in favor of an
approach that takes into account the varied and
distinct pathophysiologies of aHFs.

Box 2.

Allen L A , and O'Connor C M CMAJ 2007;176:797-805

2007 by Canadian Medical Association

Box 1.

Allen L A , and O'Connor C M CMAJ 2007;176:797-805

2007 by Canadian Medical Association

Fig. 1: Approximation of cardiac systolic function and cardiac filling pressures in various
acute illnesses.30.

Allen L A , and O'Connor C M CMAJ 2007;176:797-805

2007 by Canadian Medical Association

Box 3.

Allen L A , and O'Connor C M CMAJ 2007;176:797-805

2007 by Canadian Medical Association

:Various targets for therapies used in the management of acute

decompensated heart failure.

Allen L A , and O'Connor C M CMAJ 2007;176:797-805

2007 by Canadian Medical Association

Acute heart failure

AHF: The rapid onset of symptoms and signs secondary to
abnormal
cardiac function.
(reduced CO, tissue hypoperfusion + congestion, increase in PCWP)
1.
2.

3.

With or without previous cardiac disease.

The cardiac dysfunction can be related:
a) to systolic or diastolic dysfunction
b) to abnormalities in cardiac rhythm
c) to preload and afterload mismatch
Often life threatening and requires urgent treatment.

The Task Force on Acute Heart Failure of the European Society of

Cardiology

Acute Heart Failure :

Other Classifications
In AHF after AMI, best applied to acute denovo heart failure:

The Killip classification :

based on clinical signs and chest X-ray findings (Stage I: No heart failure, Stage II: Heart
failure, Stage III: Severe heart failure and Stage IV: Cardiogenic shock).
The Forrester classification
: based on clinical signs and haemodynamic cha-racteristics.

In a cardiomyopathy service, best applied to chronic decompensated heart failure:

Clinical severity classification :

based on observation of the peripheral cir-culation and on auscultation of the lungs for
congestion
(Class I: dry and warm, Class II: wet and cold, Class III: cold and dry and Class IV: cold and
wet).
Nohria A et al: JACC 2003;41:1797-1804.

Acute Heart Failure : Classification

The patient with AHF may present with one of several distinct clinical conditions:

Acute decompensated heart failure (de novo or as decompensation of CHF) : With

mild signs and symptoms of AHF and do not fulfil criteria for cardio-genic shock,
pulmonary oedema or hypertensive crisis.
Hypertensive acute heart failure: Signs and symptoms of HF + high BP + preserved
LVF + chest radiograph findings APO.
Pulmonary oedema: Verified by chest X-ray, severe respiratory distress, or-thopnoea
with SaO2 <90%.
Cardiogenic shock: Reduced BP (SBP<90mmHg or drop of mean AP >30mmHg)
and/or low urine output (<0.5 ml/kg/h), with pulse rate >60 bpm with or without
evidence of organ congestion.
High output failure: High CO + HR, pulmonary congestion, sometimes low BP
(arrhythmias, thyrotoxicosis, anaemia, Paget disease, iatrogenic etc)
Right heart failure: Low CO + increased jugular venous pressure + increased liver
size + hypotension.

The Task Force on Acute Heart Failure of the European Society of Cardiology

Acute Heart Failure : Classification

HR

SBP

CI

PCWP

Congestion
Killip/
Forrester

Diuresis

Hypoperfusion

End organ
hypoperfusion

+/-

Low
Normal
/
High

Low
normal /
High

Mild
elevation

K II / F II

+/-

II Acute heart
failure with
hypertension/
hypertensive crisis

Usually
increased

High

+/-

>18

K II- IV/ FII-III

+/-

+/-

+, with CNS
symptoms

III Acute heart

failure with
pulmonary oedema

Low
normal

Low

Eleva
ted

KIII/ FII

+/-

Cardiogenic
shock*:
IVa. Low output
syndrome

Low
normal

Low, <2.2

>16

K III-IV /
F I-III

low

IVb Cardiogenic
shock

>90

<90

<1.8

>18

K IV/ F IV

Very low

++

+/-

+/-

KII/FI-II

Usually
low

Low

Low

Low

FI

+/-

+/-, acute
onset

+/-

I. Acute
decompensated
congestive heart
failure*

V. High output
failure
VI. Right sided
acute heart failure

Underlying diseases and comorbidities in acute heart failure

Coronary artery disease
Valvular disease
Prosthetic valve thrombosis
Aortic dissection
AHF and hypertension
Renal failure
Pulmonary diseases and bronchoconstriction
Arrhythmias and AHF

Peri-operative

AHF

myocardial ischaemia)

(usually

due

to

Goals of treatment of the patient

with acute heart failure
Clinical

symptoms (dyspnea and/or fatigue)

clinical signs
body weight
diuresis
oxygenation

Laboratory examinations

BUN and/or creatinine

serum electrolyte normalisation
plasma BNP
blood glucose normalisation

Haemodynamic
pulmonary wedge pressure to < 18 mm Hg
cardiac output and/or stroke volume

The Task Force on Acute Heart Failure of the European Society of Cardiology

Patient with AHF: immediate treatment goals

The Task Force on Acute Heart Failure of the European Society of Cardiology

Oxygen in acute heart failure

Target SaO2 (95 98%)

Class I, LOE-C

O2 administration in hypoxaemic patients with acute heart

failure
Class IIa, LOE-C

No O2 (or FiO2) in patients without evidence of

hypoxaemia

Hyperoxia causes harm:

coronary blood flow,

cardiac output
blood
The Task Force
on Acute
Heart pressure
Failure of the European Society of Cardiology

Non invasive ventilation (NIV)

and intubation (TI) in acute heart
failure

Use of CPAP and NIPPV in acute cardiogenic

pulmonary oedema is associated with a significant
reduction in the need for endotracheal intubation (TI)
and mechanical ventilation [MV, (Class IIa, LOE-A)].

T.I. (MV) use: To reverse induced respiratory muscle

fa-tigue (low respiratory rate, hypercapnia, confusion):

a) Intervention
b) Only if acute respiratory failure does not
respond to vasodilators, O2

and/or CPAP or

NIPPV
The Task Force on Acute Heart Failure of the European Society of Cardiology

Guidelines for pulmonary artery catheter

(PAC) use in acute heart failure
Insertion of PAC for the diagnosis of acute heart failure
is usually unnecessary
PAC can be used to distinguish between a cardiogenic
and a not cardiogenic mechanism in complex patients
with concurrent cardiac and pulmonary disease.
PAC is frequently used to estimate hemodynamic
variables and guide therapy in the presence of severe
diffuse

pulmo-nary

pathology

or

ongoing

haemodynamic compromise not resolved by initial

(Class IIb, LOE-C)
therapy
The Task Force on Acute Heart Failure of the European Society of Cardiology

Non-pharmacologic Management

Surgical treatment in
acute heart failure

Chronic HF-End Stage >ADHF

Collaborative Management
Nonpharmacologic therapies (contd)
Intraaortic balloon pump (IABP) therapy
Used for cardiogenic shock
Allows heart to rest

Ventricular assist devices (VADs)

Takes over pumping for the ventricles
Used as a bridge to transplant

Destination therapy-permanent, implantable VAD

Cardiomyoplasty- wrap latissimus dorsi around heart
Ventricular reduction -ventricular wall resected
Transplant/Artificial Heart

Intraaortic Balloon Pump (IABP)

Provides temporary circulatory assistance
Afterload
Augments aortic diastolic pressure
Outcomes
Improved coronary blood flow
Improved perfusion of vital organs

Intraaortic balloon pump

IABP Machine

Enhanced External
Counterpulsation-EECP
The Cardiology Group, P.A
.

Pumps during diastoleincreasing O2 supply to

coronary arteries. Like IABP
but not invasive.

Ventricular
Assist
Devices
Ventricular
Assist
Devices
(VADs)
(VADs)

Indications for VAD therapy

Extension of cardiopulmonary bypass
Failure to wean
Postcardiotomy cardiogenic shock

Bridge to recovery or cardiac

transplantation

Copyright 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.

Patients with New York Heart Association Classification IV who

have failed medical therapy

Patient Teaching-Cleveland Clinic for Heart Fai

lure LVAD devices

Schematic Diagram of Left VAD

Left ventricular assist d

evice

HeartMate II

The HeartMate II -one of several new LVAD devices- designed to last longer with simplicity
of only one moving part; also much lighter and quieter than its predecessors; major
differences is rotary action which creates a constant flow of blood, not pumping action.

Cardiomyoplasty technique: left latissimus dorsi muscle

(LDM) transposed into chest through a window created by
resecting the anterior segment of 2nd rib (5 cm). LDM is
then wrapped around both ventricles. Sensing and pacing
electrodes are connected to an implantable cardiomyostimulator

Left Ventricular reduction Surg

ery-Bautista
procedureindicated in some
cases

Click here for UTube

Artificial Heart animination!

Surgical
treatment in
AHF:
mechanical
assist
devices and
heart
transplantat
ion
(algorithm)

Biventricular system devices

Left ventricular assist device

Paracorporeal ventricular assist device

Acute Decompensated Heart Failure

(ADHF)- Inpatient Management

Jennifer Kumar
February 2014

Objectives
Learn to identify the signs and symptoms of
ADHF
Learn to interpret pertinent laboratory data
and imaging
Learn the inpatient management of ADHF

Imaging: Chest x-ray

Enlarged cardiac silhouette

Pulmonary edema
Pulmonary congestion
Cephalization
Kerley B lines
Peri-bronchial cuffing

Pleural effusions, typically bilateral

Transition to Outpatient

Summary

Identify clinical signs and symptoms of ADHF

Pertinent labs
Sodium, creatinine, troponin, BNP

Relevant imaging
EKG, CXR, echocardiography

Treatment
Diuresis, BB, ACEI/ARB, Spironolactone, Digoxin,
Isosorbide dinitrate/Hydralazine

Transition to outpatient
Strict instructions, close-follow-up

A brief
discussion of
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PREload

AFTERload Contractility

Current Treatment of Acute Heart Failure

High
Preload
Reduce
fluid
volume

Diuretics
LASIX

High
Afterload

Poor
Contractility

Vasodilate
Augment
Contractility

VasodilatorsN
itroglycerin

Inotropes
-reduce
afterload-

Current Treatment of Acute Heart Failure

Vasodilators
Diuretics
Reduce
fluid
volume

Lasix

Decrease
Preload
And
Afterload

Lasix
Ntg: sl, top, iv
MSO4
ACEi

Vasodilate
Augment
Contractility

ACE inhibitor
Nitroglycerin

BiPAP or CPAP??
Multiple small case reports of Noninvasive
Ventilatory Support (NVS) in patients with
varying diagnoses of respiratory failure.
No assessment of hemodynamic findings in
a controlled fashion.
No assessment of neurohormonal effects of
NVS.

BiPAP vs CPAP??
Mehta. Crit Care Med 1997;25:620-628.
One small study raising concern for BiPAP-associated
AMI in pulmonary edema patients, compared to CPAP. 27
pts randomized with more rapid improvements in dyspnea
and oxygenation associated with BiPAP: BiPAP and CPAP
good, BiPAP = MI
Kosowsky. Am J Emerg Med 2000;18:91-95. Good review
of literature to date on Noninvasive Ventilatory Support
(NVS).

Effects of Nesiritide
Venous, arterial, coronary
VASODILATION
HEMODYNAMIC

NATRIURESIS
DIURESIS

CARDIAC
INDEX

rhBNP

R I SS
D
S
M
S
K
G
R
L
G
H
G
F
R
C
R
S
S
C
K V L
G
S P K MV
QGS

Preload
Afterload
PCWP
Dyspnea

RENAL

Fluid volume
Preload
Diuretic
usage

Aldosterone
Endothelin
Norepinephrine

CARDIAC
No increase in HR
Not proarrhythmic

SYMPATHETIC AND
NEUROHORMONAL SYSTEMS

2013 ACCF/AHA Guideline

for the Management of
Heart Failure
Developed in Collaboration With the American
Academy of Family Physicians, American College of
Chest Physicians, Heart Rhythm Society, and
International Society for Heart and Lung
Transplantation
Endorsed by the American Association of
Cardiovascular and Pulmonary Rehabilitation

Initial and Serial Evaluation of

the AHF Patient

Clinical Evaluation

Definition of Heart Failure

Classification

Ejection
Fraction

Description

I. Heart Failure with

Reduced Ejection Fraction
(HFrEF)

40%

Also referred to as systolic HF. Randomized clinical trials have

mainly enrolled patients with HFrEF and it is only in these patients
that efficacious therapies have been demonstrated to date.

II. Heart Failure with

Preserved Ejection
Fraction (HFpEF)

50%

Also referred to as diastolic HF. Several different criteria have been

used to further define HFpEF. The diagnosis of HFpEF is
challenging because it is largely one of excluding other potential
noncardiac causes of symptoms suggestive of HF. To date,
efficacious therapies have not been identified.

a. HFpEF, Borderline

41% to 49%

These patients fall into a borderline or intermediate group. Their

characteristics, treatment patterns, and outcomes appear similar to
those of patient with HFpEF.

b. HFpEF, Improved

>40%

It has been recognized that a subset of patients with HFpEF

previously had HFrEF. These patients with improvement or
recovery in EF may be clinically distinct from those with
persistently preserved or reduced EF. Further research is needed to
better characterize these patients.

Classification of Heart Failure

A
B

ACCF/AHA Stages of HF
At high risk for HF but without structural
heart disease or symptoms of HF.
Structural heart disease but without signs
or symptoms of HF.
Structural heart disease with prior or
current symptoms of HF.

Refractory HF requiring specialized

interventions.

NYHA Functional Classification

None
I

No limitation of physical activity.

Ordinary physical activity does not cause
symptoms of HF.

No limitation of physical activity.

Ordinary physical activity does not cause
symptoms of HF.

II

Slight limitation of physical activity.

Comfortable at rest, but ordinary physical
activity results in symptoms of HF.

III

Marked limitation of physical activity.

Comfortable at rest, but less than ordinary
activity causes symptoms of HF.

IV

Unable to carry on any physical activity

without symptoms of HF, or symptoms of
HF at rest.

Initial and Serial Evaluation of

the HF Patient

Diagnostic Tests

I IIaIIbIII

I IIaIIbIII

Diagnostic Tests
Initial laboratory evaluation of patients presenting with HF
should include complete blood count, urinalysis, serum
electrolytes (including calcium and magnesium), blood urea
nitrogen, serum creatinine, glucose, fasting lipid profile, liver
function tests, and thyroid-stimulating hormone.

Serial monitoring, when indicated, should include serum

electrolytes and renal function.

Diagnostic Tests (cont.)

I IIaIIbIII

I IIaIIbIII

I IIaIIbIII

A 12-lead ECG should be performed initially on all patients

presenting with HF.

Screening for hemochromatosis or HIV is reasonable in

selected patients who present with HF.

Diagnostic tests for rheumatologic diseases, amyloidosis, or

pheochromocytoma are reasonable in patients presenting with
HF in whom there is a clinical suspicion of these diseases.

Initial and Serial Evaluation of

the HF Patient

Biomarkers
Ambulatory/Outpatient

Ambulatory/Outpatient
I IIaIIbIII

I IIaIIbIII

In ambulatory patients with dyspnea, measurement of BNP or

N-terminal pro-B-type natriuretic peptide (NT-proBNP) is
useful to support clinical decision making regarding the
diagnosis of HF, especially in the setting of clinical uncertainty.
Measurement of BNP or NT-proBNP is useful for establishing
prognosis or disease severity in chronic HF.

Ambulatory/Outpatient
I IIaIIbIII

I IIaIIbIII

I IIaIIbIII

(cont.)
BNP- or NT-proBNP guided HF therapy can be useful to
achieve optimal dosing of GDMT in select clinically euvolemic
patients followed in a well-structured HF disease management
program.
The usefulness of serial measurement of BNP or NT-proBNP to
reduce hospitalization or mortality in patients with HF is not
well established.
Measurement of other clinically available tests such as
biomarkers of myocardial injury or fibrosis may be considered
for additive risk stratification in patients with chronic HF.

Initial and Serial Evaluation of

the HF Patient

Biomarkers
Hospitalized/Acute

Hospitalized/Acute
I IIaIIbIII

I IIaIIbIII

Measurement of BNP or NT-proBNP is useful to support

clinical judgment for the diagnosis of acutely decompensated
HF, especially in the setting of uncertainty for the diagnosis.

Measurement of BNP or NT-proBNP and/or cardiac troponin is

useful for establishing prognosis or disease severity in acutely
decompensated HF.

Hospitalized/Acute
(cont.)
I IIaIIbIII

I IIaIIbIII

The usefulness of BNP- or NT-proBNP guided therapy for

acutely decompensated HF is not well-established.

Measurement of other clinically available tests such as

biomarkers of myocardial injury or fibrosis may be considered
for additive risk stratification in patients with acutely
decompensated HF.

Treatment of Stages A to D

Mechanical Circulatory
Support

Coronary Artery Bypass Graft

Surgery

CABG in Patients With

STEMI

CABG in Patients With STEMI

I IIaIIbIII

I IIaIIbIII

Urgent CABG is indicated in patients with STEMI

and coronary anatomy not amenable to PCI who have
ongoing or recurrent ischemia, cardiogenic shock,
severe HF, or other high-risk features.
CABG is recommended in patients with STEMI at
time of operative repair of mechanical defects.

CABG in Patients With STEMI

I IIaIIbIII

I IIaIIbIII

The use of mechanical circulatory support is

reasonable in patients with STEMI who are
hemodynamically unstable and require urgent CABG.
Emergency CABG within 6 hours of symptom onset
may be considered in patients with STEMI who do
not have cardiogenic shock and are not candidates for
PCI or fibrinolytic therapy.

Heart failure syndromes

Forward HF
Weakness, confusion, low BP
Vasodilation, fluid replacement, inotropic
support

LV intropy, SV, CO, PAOP

Heart failure syndromes

left ventricular dysfunction
Left-backward HF
DOE, pulmonary edema, BP normal or high
Vasodilation, diuretics, bronchodilators (?),
respiratory support (?)

LV intropy, SV, CO, PAOP

Acute right heart failure results

from pulmonary and right heart
dysfunction
Right backward HF
Peripheral edema, dyspnea, and ascites
Diuretics for fluid overload
Fluids for RV infarction

RV intropy, +/- PAOP

AHA/ACC Guideline
2014 AHA/ACC Guideline for the Management of Patients With Valvular
Heart Disease
A Report of the American College of Cardiology/American Heart Association
Task Force on Practice Guidelines
Rick A. Nishimura, MD, MACC, FAHA,

A brief
discussion of
the works of
this thing...