Download Acute heart failure syndromes and cardiogenic shock

CURRENT STATUS OF ADHF
TREATMENT IN 2015
Prof. Dr. Dilek Ural
The year in AHF - 2015
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2005 2006 2007 2008 2009 2010 2011 2012 2013 2014 2015
Pubmed: “acute heart failure”
The year in AHF - 2015
Contents
Definitions
Epidemiology
Clinical Evaluation and Diagnostic Approach
Management in ED/CCU/Ward
Contents
Definitions
Epidemiology
Clinical Evaluation and Diagnostic Approach
Management in ED/CCU/Ward
Definition



Acute heart failure (AHF) is defined as a life
threatening clinical syndrome with rapidly
developing or worsening typical heart failure (HF)
symptoms and signs requiring emergent treatment.
Worsening (decompensated) HF – Preexisting and
stable HF that worsens suddenly or progressively is
described as decompensated AHF.
New (de novo) HF - There is no known previous HF.
Symptoms and findings appear suddenly after an
acute event [e.g. acute myocardial infarction (AMI)]
or gradually in the presence of asymptomatic left
ventricular systolic and/or diastolic dysfunction.
In-hospital worsening heart failure
Frequency of in-hospital worsening heart failure: 4.5-30%. Mortality is ~19% in 30-day and 50%
in 1-year compared to 7.3% and 32.7%, respectively, in those with an uncomplicated course.
In-hospital worsening renal function
Frequency of in-hospital worsening renal function: 20-30%, sign of increaed 90-day mortality.
In-hospital events
Worsening heart failure
Worsening renal function
Ischemic hepatitis
Congestive hepatopathy
Failure to improve or worsening signs and symptoms of
HF despite therapy that occurs
1-2 days (usually in the first 7 days) after
hospitalization and
requires initiation or intensification of parenteral
therapy [e.g. inotropes or vasoactive agents] or
implementation of mechanical cardiac or ventilatory
support.
Increase in serum creatinine of ≥0.3 mg/dL or decrease
in eGFR ≥25% after admission.
Decreased blood supply (due to shock or low blood
pressure) to liver resulting in liver injury and marked
elevation of liver function tests
Liver dysfunction due to venous congestion, usually right
heart failure
Contents
Definitions
Epidemiology
Clinical Evaluation and Diagnostic Approach
Management in ED/CCU/Ward
Clinical Characteristic of Acute Heart
Failure Patients in Different Registries

AHF is reported as the cause of hospitalization in 20% of cases older than 65 years.

About 30–50% of the AHF patients have preserved LVEF.
I n-hospital mortality rate of AHF is similar to AMI and ranges between 4–7% in registry studies.

Farmak,s D, et al. Rev Esp Cardiol. 2015;68:245–248
Data of patients on hospital admissions
at TAKTIK and other registry studies
Mean age (years)
Female (%)
New onset HF (%)
CAD (%)
Hypertension (%)
Diabetes (%)
Atrial fibrillation (%)
COPD (%)
CRF (%)
SBP (mmHg)
SBP < 90 mmHg (%)
SBP 90-140 mmHg (%)
SBP >140 mmHg (%)
Peripheral edema (%)
Cold extremities (%)
ACS (%)
Arrhythmias (%)
Valvular disease (%)
Infection (%)
Non-compliance to treatment (%)
Hemoglobin (g/dL)
Creatinine (mg/dL)
Troponin I (mg/dL)
Left ventricular EF (%)
EF >% 40 (%)
Diuretic (%)
ACE-I (%)
Beta-blocker (%)
ARB (%)
MRA (%)
Digoxin (%)
In hospital mortality (%)
TAKTIK
(n=558)
62±13
38
24
61
53
40
32
20
16
125±28
3
78
19
65
34
29
30
46
22
34
12.4±2.1
1.4±0.9
2.2±9
33±13
20
62
50
46
10
40
4
3.4
EHFS-II
(n=3.580)
70±13
39
37
54
63
33
39
19
17
2
48
50
23
30
32
27
18
22
38±15
34 (>%45)
71
55
43
9
28
26
6.7
ADHERE
(n=105.388)
72±14
52
23
57
73
44
31
31
30
144±33
1
70
29
66
12.4±2.7
1.8±1.6
34±16
37
41
70
48
12
9
28
4
OPTIMIZE-HF
(n=48.612)
73±14
52
12
50
71
42
31
28
20
143±33
8
44
48
85
15
14
15
9
12.1±3.4
1.8±1.8
0.1 (median)
39±18
51
66
40
53
12
7
23
3.8
Data of patients on hospital admissions
at TAKTIK and other registry studies
Mean age (years)
Female (%)
SBP < 90 mmHg (%)
SBP 90-140 mmHg (%)
SBP >140 mmHg (%)
Non-compliance to treatment (%)
EF >% 40 (%)
Diuretic (%)
ACE-I (%)
Beta-blocker (%)
ARB (%)
MRA (%)
Digoxin (%)
In hospital mortality (%)
TAKTIK
(n=558)
62±13
38
3
78
19
34
20
62
50
46
10
40
4
3.4
EHFS-II
(n=3.580)
70±13
39
2
48
50
22
34 (>%45)
71
55
43
9
28
26
6.7
ADHERE
(n=105.388)
72±14
52
1
70
29
37
41
70
48
12
9
28
4
OPTIMIZE-HF
(n=48.612)
73±14
52
8
44
48
9
51
66
40
53
12
7
23
3.8
Usage of ACE-I increased from 50% on admission to 54% at discharge, beta-blockers
increased from 46% to 57%, and aldosterone antagonists from 40% to 52%. The only agent
that was prescribed more than on admission was digoxin with an increase from 4% to 33%.
Contents
Definition
Epidemiology
Clinical Evaluation and Diagnostic Approach
Management in ED/CCU/Ward
Precipitating causes
Cardiac
Treatment noncompliance:
1. Salt and fluid intake
2. Non-compliance with drug treatment
Ischemic Heart Disease:
1. Acute coronary syndrome
2. Mechanical complications of AMI
3. Right ventricular MI
Valvular Heart Disease:
1. Valvular stenosis
2. Valvular regurgitation
3. Endocarditis
4. Aortic dissection
Cardiomyopathies:
1. Peripartum CMP
2. Acute myocarditis
3. Pericardial tamponade
Hypertensive/Arrhythmic:
1. Hypertension
2. Acute arrhythmias (e.g. AF, tachyarrhythmias,
serious bradycardia, etc.)
Concomittant usage of negative inotropic drugs:
Verapamil, beta-blockers, diltiazem, nifedipine, etc.
Non-Cardiac
Endocrinological diseases:
Diabetes, thyrotoxicosis, hypothyroidism, etc.
Pulmonary diseases:
Pulmonary emboli, asthma, COPD
Infections:
Pneumonia, influenza, sepsis, etc.
Cases increasing blood volume:
Anemia, shunts, beriberi, Paget disease
Renal failure
Drugs and addictions:
Drugs leading to sodium retention (e.g. steroids,
tiazolidinediones, NSAI's), excessive alcohol or
illegal drug addiction
Others:
Cerebrovascular event, surgical intervention
Symptoms and signs
The main symptoms which dominates clinical
presentation is related to the systemic and pulmonary
congestion.
1. Pulmonary congestion:
The accumulation of an abnormal amount of blood in
the vascular bed of the lungs. It usually occurs in asso
ciation with left heart failure.
2. Systemic congestion: Congestion of the subsidiary
organs of the systemic circulation as a result of right
heart failure. The main symptoms are edema, venous
congestion in the lower extremities, liver and spleen,
liver and splenic congestion, and engorgement jugular.

Demographical and clinical characteristics
of 5 clinical scenarios of AHF
Diagnostic tests

Chest X ray
Enlarged heart silhouette, pulmonary
congestion, pleural effusion, Kerley
lines pulmonary interstitial or alveolar
edema.
A normal chest radiogram (observed
in ~20% of cases) does not exclude
AHF diagnosis.
 ECG
ECG should be performed at initial
evaluation in all AHF patients and
cardiac rhythm should be monitored.
ECG is almost always abnormal in
patients admitted with acute
decompensated HF.
Diagnostic tests
Hemogram
Blood glucose
Urea, creatinine,
BUN and estimated
eGFR
Creatinine and electrolytes should be monitored at short intervals
(daily during IV treatment, in 1-2 days after starting oral treatment)
during AHF treatment.
Electrolytes
Transaminases
Liver function abnormalities are detected in about 75% of AHF
patients and are closely related to the severity of disease and clinical
findings.
C-reactive protein
Myocardial injury
biomarkers
Increase in troponin is observed in 30-50% of cases (even without
myocardial infarction)
BNP or NT-proBNP
- Initial evaluation of suspected AHF
- Patients with ongoing symptoms in CCU/ward
-Prior to discharge
Diagnostic tests
Echocardiography: Differential diagnosis Thoracic ultrasonography: Pulmonary
and to plan treatment of AHF.
congestion. B lines in congestion (comet
tails) whereas A lines chronic obstructive
If can be performed in ED, it provides
pulmonary disease.
information about etiology of AHF,
cardiac anatomy (e.g. volumes, geometry,
mass) and functions.
A
lines
B-lines arise from the pleural line,
creating a pattern called lung rockets.
These vertical, long, well-defined
artifacts erasing the A-lines and
moving in concert with lung sliding
indicate the changeover from below
to above 18 mm Hg when this pattern
replaces A-lines during fluid therapy.
Contents
Definition
Epidemiology
Clinical Evaluation and Diagnostic Approach
Management in ED/CCU/Ward
Management of AHF
Main objectives of AHF treatment are symptomatic relief and hemodynamic
recovery.
Other initial treatment objectives are improving oxygenation to required levels
(PaO2 >60 mm Hg, SpO2 >90%), restriction of organ damage and decreasing
duration of stay in intensive care unit.
Management in Emergency Department


Venous line
Monitorization




ECG: Baseline
and follow-up
SaO2 monitorization (pulse
oxymeter): If < 90%
administer nasal oxygen (with
cannula or mask; goal: >95%)
Blood pressure (Invasive
continuous [arterial line], noninvasive, 5 minute apart).
Urine output
Invasive hemodynamic monitorization
Swan-Ganz (pulmonary artery) catheterization, which had been used more
frequently in former years, is currently recommended only in selected cases, as it
does not add more information to those obtained by non-invasive methods.
Patients who would benefit from hemodynamic monitorization are:
(i) patients with hypotension/cardiogenic shock who don't respond to fluid treatment,
(ii) ACS patients with mechanical complications,
(iii) cases not responsive to standard treatment, and measurement of intravascular volume,
cardiac output and pulmonary capillary wedge pressure will be beneficial in planning the
treatment,
(iv) cases who are candidates for heart transplantation or implantation of a LVAD.
Intra-arterial catheterization is used to monitor mean arterial pressure in patients
with low SBP in whom signs of AHF don't improve morbidity or mortality. It is also
beneficial for patients who receive vasopressor treatment and in whom arterial
blood gas analysis should be repeated frequently.
Management in Emergency Department


Diuretic treatment: Furosemide 20-40 mg IV bolus
Diuretic response (urine output >100 mL/h in first two hours,
relief of dyspnea) should be waited after this initial dose.
Vasoactive treatment : In patients with a SBP >110-120 mmHg,
time between first admission and initiation of IV nitrates should
not be more than 2 hours. Sublingual or oral nitrate treatment
instead of parenteral forms of vasodilators can be preferred for
patients with relatively less serious symptoms and findings in
emergency unit.
Management in Emergency Department

Routine opioid administration: There is no strong
evidence supporting benefits of routine use. Morphine at
a dose of 4-8 mg can be applied with
metoclopropamide (morphine induces nausea) in patients
with significant anxiety, then again respiration should be
monitored carefully.
Triage into CCU/ICU





Patients with a respiratory rate >25/min,
SaO2 <90% or requiring intubation,
Systolic BP <90 mm Hg,
Hypoperfusion findings (existence of any: lactate >2
mmol/L, confusion, metabolic acidosis, oliguria, cold
extremities in room temperature, mixed venous oxygen
saturation <65%) should be directed into CCU/ICU.
Patients without critical findings can be followed in ward
and receive treatment including parenteral drugs.
Triage: Discharge to home
Approximately half of AHF patients can be discharged
from emergency department.
 Patients subjectively mentioning she/he has recovered,
 Resting heart rate <100/min,
 Room air oxygen saturation ≥95%,
 Urine output >30 cc/h,
 No orthostatic hypotension or end organ dysfunction are
potential candidates for early discharge.
These rules are not valid for de novo AHF patients who
should always be hospitalized.
Management in ICU/CCU


Fluid and sodium restriction – Although a strict fluid restriction is
not recommended, a fluid intake of 1.5-2 L/day is commonly
recommended for AHF patients (especially for hyponatremic cases)
to relieve symptoms and congestion during the initial management.
Sodium restriction (to 2‒3 g/day) may also help to control the
symptoms and signs of congestion. Nonetheless, there is no clear
evidence to support these recommendations.
Venous thromboembolism prophylaxis – Hospitalization due to
AHF carries a high risk for development of venous thromboembolism.
Therefore prophylactic anticoagulation (enoxaparin 40 mg
subcutaneously once daily or unfractionated heparin 5000 units 3
times/day subcutaneously) is recommended for patients during the
hospital stay. However, evidence from randomized clinical trials are
lacking for this recommendation.
Ventilation
Indications for noninvasive ventilation
1.
2.
3.
4.
5.
6.
Inadequate response to initial standard therapy
High-risk of endotracheal intubation
Respiratory rate ≥30/min
Persistent O2 saturation ≤ 90% or PaO2/FiO2 <200 mmHg on >4 L/min oxygen
Mild hypercapnia (CO2 <45 mmHg) or acidosis (pH <7.3)
Respiratory muscle fatigue
FiO2 = fraction of inspired oxygen, PaO2 = partial pressure arterial oxygen.
A-CPAP settings:
• Start with 5- H2O
• Increase in increments of H2O, as tolerated and indicated
• FiO2 >40%
B-BIPAP settings:
• Initial inspiratory pressure of 8–10 cm H2O
• Increase in increments of 2–4 cm H2O (Max ~20 cm
H2O) aiming at tidal volume >7ml/kg
• Initial expiratory pressure of ~4- H2O
• Maximum inspiratory pressure is H2O and expiratory
pressure H2O
• FiO2 >40%
Ventilation
Indications for endotracheal ventilation
Any 1 of the following:
• pH less than 7.20
• pH 7.20–7.25 on 2 occasions 1 hour apart
• Hypercapnic coma (Glasgow Coma Scale
score < 8 and PaCO2 >60 mm Hg)
• PaO2 less than 45 mm Hg
• Cardiopulmonary arrest
Two or more of the following in the context
of respiratory distress:
• Respiratory rate >35 breaths/min or <6
breaths/minute
• Tidal volume <5 mL/kg
• Blood pressure changes, SBP <90 mm Hg
• SaO2 <90% despite adequate
supplemental oxygen
• Hypercapnia (PaCO2 >10 mm increase) or
acidosis (pH decline >0.08) from baseline
• Obtundation
• Diaphoresis
• Abdominal paradox
Treatment approach according
to systolic blood pressure
Diuretics


IV bolus administration of loop diuretics (approximately 2.5 times the
outpatient dose should be considered) may be followed by continuous IV
infusion.
Urine output should be increased to ≥40 mL/h and a weight loss of 1-1.5
kg/day should be achieved. Patient’s BP, fluid balance, weight at the same
hour of each day (preferably in the morning), daily renal functions and
electrolytes should be monitored as long as parenteral treatment continues.
Furosemide
20 – 80 mg bolus
20 – 500 mg bolus
Continious infusion
* 5 – 40 mg / h
* 0.1 – 0.5 mg / h
* 5 – 20 mg / h
**Ototoxicicity in high dosages
Bumetanide **
0.5 – 2 mg bolus
0.5 – 4 mg bolus
Continious infusion
* 0.1 – 0.5 mg / h
Torsemide **
10 – 40 mg bolus
20 – 200 mg bolus
Continuous infusion
* 5 – 20 mg / h
Vasodilators


In the absence of hypotension (SBP >110 mmHg) vasodilators can be used
as the first-line agents in combination with diuretics.
Most useful in patients with hypertension.
IV
Initial dose
Effective dose range
Comments
Nitroglyserin
20 μg /min
40 – 400 μg / min
* Hypotension and headache
* Tolerance with 24 h of continious infusion
Nitroprusside
10 μg / min
30 – 350 μg / min
0.3 – 5 μg / kg / min
*< 4μg/kg/min
* Caution in patients with ischemia
* Hypotension
* Cyanide side effect (nausea)
* Thiocyanate toxicity, light sensitivity
Nesiritide **
2 μg / kg bolus
Infusion 0.010.03 μg/kg/min
0.01-0.03 μg/kg/min
* 1 μg / kg bolus, 0.005 μg / kg / mininf.
* Hypotension, headache
( B type natriüretic peptid)
Inotropes





Use of an inotrope should be limited to patients with

Dilated ventricles and reduced EF

Low SBP (<90 mmHg) or low measured CO

In the presence of signs of vital organ hypoperfusion (reduced urine output).
Should be used temporarily with close monitoring of rhythm and
hemodynamic parameters.
May increase mortality by inducing arrhythmias and by increasing
myocardial O2 requirement (positive inotropic and chronotropic).
Should be stopped as soon as adequate organ perfusion is
restored.
May be used in cardiogenic shock as a temporary treatment to
prevent hemodynamic collapse.
Inotropes
1 – 2 μg / kg /min
2 – 20 μg / kg / min
* For inotropy ve vasodilation
* Hypotension, tachycardia, arrhythmias
1 – 2 μg / kg / min.
2 – 4 μg / kg / min
Putative effect on
renal vasodilation
4 – 5 μg / kg / min.
5 – 20 μg / kg / min
* For inotropy ve vasodilation
* Hypotension, tachycardia, arrhythmias
* For inotropy ve vasocnstruction
* Tachycardia, arrhythmias
Milrinone **
0.10 – 0.75 μg / kg / min.
PDEI
25 – 75 μg / kg bolus –
over 10 – 20 min.,
followed by infusion
* For inotropy ve vasodilation
* Hypotension, tachycardia, arrhythmias
Enoximone **
0.25 – 0.75 mg / min
1.25 – 7.5 μg / kg / min.
* For inotropy ve vasodilation
* Hypotension, tachycardia, arrhythmias
12 – 24 μg / kg bolus
over 10 min. + infusion
0.5 – 2.0 μg / kg / min.
* For inotropy ve vasodilation
* Hypotension, tachycardia, arrhythmias
0.05 – 0.5μg / kg / min.
* For inotropy ve vasocnstruction
* Tachycardia, arrhythmias, end-organ
hypoperfusion
0.2 – 1.0 μg / kg / min
* For inotropy ve vasocnstruction
* Tachycardia, arrhythmias, end-organ
hypoperfusion
Dobutamine
Β Agonist
Dopamine
Β + α Agonist
PDEI
Levosimendan
Ca sensitizer
Epinephrine
Full β Agonist
Norepinephrine
Adr. Agonist
Ultrafiltration


Peripheral ultrafiltration
is an available modality
to remove sodium and
water in patients
resistant to routine IV
diuretic therapy.
Ultrafiltration is used to
remove isotonic fluid
resulting in greater and
more reliable salt
removal.
Management in ward
Short-term objectives during the hospital stay include
 Stabilization of clinical status by optimal treatment,
 Starting appropriate oral pharmacological treatment,
 Consideration of device treatment in selected cases
and
 Decreasing hospital stay.
Scales for evaluation of dyspnea in
AHF
Management in CCU/ward

Treatment algorithms according to clinical scenarios (CS)
CS 1: AHF presenting with hypertension accompanied by
dyspnea and/or congestion
 CS 2: AHF presenting with normal SBP accompanied by
dyspnea and/or congestion
 CS 3: AHF presenting with hypotension, dyspnea and other
congestion symptoms
 ClS 4: AHF complicating acute coronary syndromes
 CS 5: Acute right HF


Cardiorenal syndrome
Preparation for discharge