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Transcript
‫المقاربات التشخيصية و العالجية‬
‫في قصور القلب‬
‫إعداد‬
‫د ‪ 0‬عمر الق اسم‬
Heart failure
Definition
It is the pathophysiological process in which
the heart as a pump is unable to meet
the metabolic requirements of the tissue for
oxygen and substrates despite the venous
return to heart is either normal or increased
Essential functions of the heart are secured
by integration of electrical and mechanical
functions of the heart
Cardiac output (CO) = heart rate (HR) x stroke vol.(SV)
- changes of the heart rate
- changes of stroke volume
Control of HR:•
- autonomic nervous system
- hormonal(humoral) control
Control of SV: •
- preload
- contractility
- afterload
Preload
Stretching the myocardial fibers during diastole by increasing enddiastolic volume  force of contraction during systole = Starling´s
law
preload = diastolic muscle sarcomere length leading to incr
tension in muscle before its contraction
venous return to the heart is important  end-diastolicvolume is influenced
stretching of the sarcomere maximises the number
of actin-myosin bridges responsible for development of force
- optimal sarcomere length  2.2 m
Afterload
It is expressed as tension which must be developed in the wall of ventricles
during systole to open the semilunar valves and eject blood to
aorta/pulmunary artery
Laplace law:
intraventricular pressure x radius of ventricle
wall tension = -------------------------------------------------------2 x ventricular wall thickness
 afterload: due to - elevation of arterial resistance
-  ventricular size
- myocardial hypotrophy
 afterload: due to -  arterial resistance
- myocardial hypertrophy
-  ventricular size
Myocardial contractility
Contractility of myocardium
Changes in ability of myocardium to develop the force
by contraction that occur independently on the
changes in myocardial fibre length
Mechanisms involved in changes of contractility
 amount of created cross-bridges in the sarcomere
by  of Ca ++i concentration
- catecholamines  Ca++i  contractility
- inotropic drugs  Ca++i  contractility
 contractility  shifting the entire ventricular function
curve upward and to the left
 contractility  shiffting the entire ventricular function
curve (hypoxia, acidosis) downward and to the right
Causes of heart pump failure
A. MECHANICAL ABNORMALITIES
1. Increased pressure load
– central (aortic stenosis, aortic coarctation...)
– peripheral (systemic hypertension)
2. Increased volume load
– valvular regurgitation
– hypervolemia
3. Obstruction to ventricular filling
– valvular stenosis
– pericardial restriction
B. MYOCARDIAL DAMAGE
1. Primary
a) cardiomyopathy
b) myocarditis
c) toxicity (e.g. alcohol)
d) metabolic abnormalities (e.g. hyperthyreoidism)
2. Secondary
a) oxygen deprivation (e.g. coronary heart disease)
b) inflammation (e.g. increased metabolic demands)
c) chronic obstructive lung disease
C. ALTERED CARDIAC RHYTHM
1. ventricular flutter and fibrilation
2. extreme tachycardias
3. extreme bradycardias
Risk Factors for Heart Failure
Coronary artery disease
Hypertension (LVH)
Valvular heart disease
Alcoholism
Infection (viral)
Diabetes •
Congenital heart defects •
Other: •
Obesity –
Age –
Smoking –
High or low hematocrit level –
Obstructive Sleep Apnea –
.
Classification of Heart Failure
ACCF/AHA Stages of HF
NYHA Functional Classification
A
At high risk for HF but without structural
heart disease or symptoms of HF.
None
B
Structural heart disease but without signs
or symptoms of HF.
I
No limitation of physical activity.
Ordinary physical activity does not cause
symptoms of HF.
C
Structural heart disease with prior or
current symptoms of HF.
I
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.
D
Refractory HF requiring specialized
interventions.
Types of Heart Failure
Classification
I. Heart Failure with
Reduced Ejection Fraction
(HFrEF)
Ejection
Fraction
≤40%
II. Heart Failure with
≥50%
Preserved Ejection Fraction
(HFpEF)
Description
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.
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.
Characteristics of Patients with Reduced and Preserved LVEF
Baseline Variables
Mean LVEF %
Age-years
Female (%)
Coronary artery disease (%)
Angina (%)
Prior myocardial infarction (%)
Prior CABG (%)
Hypertension (%)
Diabetes (%)
Atrial Fibrillation (%)
COPD (%)
Hemoglobin <10 g/dl (%)
Systolic blood pressure-mm Hg
Reduced EF
Preserved EF
P-value
(<40%, n=1570)
(>50%, n = 880)
25.9
62.4
<0.001
71.8 ± 12
75.4 ± 11.51
<0.001
37.4
48.7
28.0
39
65.7
35.5
22.8
16.6
12.9
84
38.9
23.6
13.2
9.9
146
5.8
91
31.7
31.8
17.7
21.1
156
<0.001
<0.001
<0.005
<0.001
<0.001
<0.001
<0.001
<0.001
<0.002
<0.001
<0.001
Bhatia et al. NEJM 2006;355:251-9
HFPEF is defined by heart failure symptoms with a normal
or near-normal EF (>0.50 or 0.45).
This cut point does not exclude mild systolic dysfunction.
The term “preserved ejection fraction” is preferred
because ejection fraction is what is commonly
measured.
HF-PEF is often equated with diastolic heart failure.
Prevalence of Heart Failure
USA
10
prevalence %
9
(CHS)
8.8
Finland
(Helsinki)
England
(Poole)
Sweden
(Vasteras)
Den.
(Copen.)
Portugal
(EPICA)
Nether.
(Rotter.)
Proportion with reduced
LV ejection fraction
8.2
8
Spain
(Asturias)
7.5
6.7
7
6.4
Proportion with preserved
LV ejection fraction
6
4.9
5
4.2
4
3
2.1
2
1
4.8
4.2
5.1
3.1
4.5
2.9
1.7
1.5
70-84
75
> 50
> 40
>25
55-95
76
75
-
60
68
65
0
age range
mean age
66-103 75-86
78
-
Diagnosis
Diagnosis is difficult
Symptoms, signs and investigations
Symptoms in the diagnosis of heart failure
Specificity %
% Sensitivity
52
81
76
80
66
21
33
23
Symptom
Dyspnoea
Orthopnoea
PND
Oedema
Signs in the diagnosis of heart failure
Specificity
Sensitivity
98
77
17
29
99
80
Clinical findings
24
20
Raised JVP
Crackles
Gallop
Oedema
DIAGNOSIS OF HF-PEF
Symptoms and clinical signs of HF
Absence of a major co-morbid condition that mimics an HF
presentation (CKD, COPD, Anemia)
Echocardiographic abnormalities: increased LV Mass, LA
size, Doppler parameters of diastolic dysfunction
Elevated Natriuretic Peptides
CXR in the diagnosis of heart failure:
Cardiothoracic ratio > 50% is specific, not sensitive
Useful to exclude other causes of SOB
Imaging: Echo
Typically repeated no sooner than annually
Provides information regarding;
Ejection fraction
Diastolic dysfunction
Wall motion abnormalities
Chamber sizes
Pulmonary HTN
Ventricular dysynchrony
BNP and the diagnosis of heart failure
BNP as a screening tool for HF in 1o care
76 / 97%
84 / 87%
70 / 16%
98 / 98%
Sensitivity
Specificity
PPV
NPV
BNP /NT proBNP levels
+ with age or female
- with obesity
+ in CKD
+ in raised pulmonary artery pressure COPD, PE, cor
pulmonale
+ in AF
+ in valvular heart disease – MR , AS, MS
+ in sepsis
+ in pericardial disease
Heart Failure Treatments:
Medication Types
What it does
Type
ACE inhibitor •
(angiotensin-converting
enzyme)
Expands blood vessels which lowers •
blood pressure, neurohormonal
blockade
ARB (angiotensin receptor •
blockers)
Similar to ACE inhibitor—lowers •
blood pressure
Beta-blocker•
Reduces the action of stress •
hormones and slows the heart rate
Digoxin•
Slows the heart rate and improves the •
heart’s pumping function (EF)
Diuretic•
Filters sodium and excess fluid from the •
blood to reduce the heart’s workload
Aldosterone •
blockade
Blocks neurohormal activation and controls •
volume
ACE I/ARB: How to do it
WHO
All patients with HF
Care: K+ > 5.5 or Cr >200 or Ur >12 or Na 130 or SBP <
100 or > frusemide 80 mg od
WHEN
Once HF confirmed (Ideally echo LV function)
HOW
Stop K+ supp and NSAID and warn re hypotension
U&E’s/K+ week 1 and 4 and ? 6 monthly after
Low dosemid 1/52. Target dose 1/12
Refer if adverse effects as above
Beta-blockers: How to do it
WHO: •
For all with mild/moderate HF (NYHA II/III) –
HR>60 SBP>100 –
Clinically stable >4/52, no AMI/UA >3/12 –
WHEN •
Once Euvolaemic –
HOW •
Bisoprolol 1.25 (1/52) 2.5(1/52)3.75(1/52) –
5 (4/52) 7.5 (4/52) 10 mg
Spironolactone: How to do it
WHO
All patients with moderate/severe HF –
Care K+ > 5.0 or Cr >221 –
WHEN •
Once stabilized on ACE I –
HOW •
Dose 25 mg/day –
U&E’s/K+ week 1 and 4 and ? 3-6 monthly after –
ICD indications in 2014
Non – ischaemic cardiomyopathy
NSVT / VT STIM no longer criteria
ICD for high risk with normal QRS duration
EF < 35% (rather than 30%) •
ICDs, Biventricular Pacemakers and
Combined CRT-D
Given NICE guidance and based on
contemporary evidence there are going to be
a lot more complex devices implanted into
patients with HF due to LV systolic dysfunction
Estimates of increase of 2x more patients
receiving devices
Who is going to pay? – at present Specialist
Commissioning Group – but they are trying to
pass back to CCG
NICE GUIDANCE 2014
ANY HEART FAILURE, LVEF ≤ 35%
QRS duration
NYHA 1
NYHA2
NYHA3
NYHA4
<120ms
ICD IF THERE IS A HIGH RISK OF SCD
NO DEVICE
120-149ms, no
LBBB
ICD
ICD
ICD
CRT-P
120-149ms with
LBBB
ICD
CRT-D
CRT-P/D
CRT-P
≥ 150ms
CRT-D
CRT-D
CRT-P/D
CRT-P
Summary
HF is increasingly prevalent.
Diagnosis is problematic use BNP and Echo.
Strong evidence base for the treatment of HF (ACE
I, BB, SPIRO).
New Drug – ACE receptor blocker and neprolysin ARB, & Digoxin cautiously.
Increasing use of Complex Device therapy.
Need more Community heart failure nurses – just
appointed a hospital based specialist nurse in HF
– to improve discharge and reduce readmission
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