Transcript قصور القلب - أسباب وتشخيص

HEART FAILURE
DR ZIAD NOFAL
CARDIOLOGIST
DAMASCUS HOSPITAL
heart failure
outlines
– Definition
– Causes and pathophysiology
– Clinical manifestations
– Classification of heart failure
– Diagnostic evaluation
– Medical management
Heart Failure Definition
• A complex clinical syndrome that can result from any
structural or functional cardiac disorder that impairs the
ability of the ventricle to fill with or eject blood.
• Cardinal manifestations are dyspnea and fatigue (which
may limit exercise tolerance), and fluid retention (which
may lead to pulmonary congestion and peripheral edema).
Hunt SA et al. J Am Coll Cardiol. 2005; 46: e1-e86.
Prevalence
• Framingham Heart Study found a prevalence
of HF in men of 8 per 1000 at age 50 to 59
years, increasing to 66 per 1000 at ages 80 to
89 years. similar values (8 and 79 per 1000)
were noted in women .
• The prevalence in African-Americans is
reported to be 25 percent higher than in whites.
Cardiovascular Deaths
300,000 death/yr
Mode of Death by NYHA Class
NYHA II
Other 24%
HF
12%
NYHA III
Other 15%
SD
64%
HF
26%
MERIT-HF Study Group. Lancet. 1999; 353: 2001-2007.
NYHA IV
Other 11%
SD
59%
SD
33%
HF
56%
heart failure
outlines
– Definition
– Causes and pathophysiology
– Clinical manifestations
– Classification of heart failure
– Diagnostic evaluation
– Medical management
Italian registry of over 6200
unselected outpatients with HF
•
•
•
•
•
Ischemic heart disease — 40 percent
Dilated cardiomyopathy — 32 percent
Primary valvular heart disease — 12 percent
Hypertensive heart disease — 11 percent
Other — 5 percent
Causes of systolic heart failure
• Coronary artery disease
• High blood pressure
• Heart valves disorders
• Inflammation
of
Heart
muscle
(myocarditis, cardiomyopathy)
Causes of diastolic heart failure
Coronary artery disease.
High blood pressure.
Hypertrophic obstructive
cardiomyopathy .
Restrictive cardiomyopathy.
Diastolic dysfunction
• The most common conditions associated
with diastolic dysfunction are aging ,
hypertension, diabetes mellitus, left
ventricular hypertrophy, coronary
disease, and infiltrative
cardiomyopathies.
Left ventricular hypertrophy
• Whether due to hypertension, coronary
disease, valve disease, or diabetes, left
ventricular hypertrophy (LVH) is a prominent
feature of evolving HF.
• Among patients with HF in the general
population, antecedent evidence of LVH is
present in approximately 20 percent by ECG
and 60 to 70 by echocardiogram.
Stage B (cont.)
I IIaIIbIII
I IIaIIbIII
In patients with structural cardiac abnormalities, including LV
hypertrophy, in the absence of a history of MI or ACS, blood
pressure should be controlled in accordance with clinical practice
guidelines for hypertension to prevent symptomatic HF.
ACE inhibitors should be used in all patients with a reduced EF to
prevent symptomatic HF, even if they do not have a history of MI.
I IIaIIbIII
Beta blockers should be used in all patients with a reduced EF to
prevent symptomatic HF, even if they do not have a history of MI.
NHANES I
•
•
•
•
•
•
Coronary heart disease — relative risk 8.1
Cigarette smoking — relative risk 1.6
Hypertension — relative risk 1.4
Overweight — relative risk 1.3
Diabetes — relative risk 1.9
Valvular heart disease — relative risk 1.5
however, valve disease is an increasingly
common cause of HF at older ages, with calcific
aortic stenosis being the most common disorder
requiring surgery
New Classification of Heart Failure
Stage
Patient Description
A
High risk for developing heart Hypertension •
CAD •
failure (HF)
B
Asymptomatic HF
C
Symptomatic HF
D
Refractory
end-stage HF
Hunt SA et al. J Am Coll Cardiol. 2005; 46: e1-e86.
Diabetes mellitus •
Family history of cardiomyopathy •
Previous MI •
LV systolic dysfunction •
Asymptomatic valvular disease •
Known structural heart disease •
Shortness of breath and fatigue •
Reduced exercise tolerance •
Marked symptoms at rest despite maximal •
medical therapy (eg, those who are recurrently
hospitalized or cannot be safely discharged from
the hospital without specialized interventions)
Role of Inflammation in HF
- One belief is that the progression of HF is heavily influenced by inflammation.
-Proinflammatory cytokines ( CRP, TNF, interleukin 6) produce toxins that directly affect the
heart and peripheral vasculature.
- In response to cardiac stress such as a myocardial infarction (MI), increased pressure or volume
overload, myocardial cells produce cytokines especially TNF
Secretes
more
cytokines
Tissue
Release of
Attract monocytes -> mature
Releases
damage,
cytokines
into macrophages
toxins
infection
(TNF, IL 6)
Decreased CO HF
Remodeling
(hypertrophy,
dilation)
Increased workload on
heart to meet body
needs
Kills
cardiomyocytes
Role of genetics in HF
-Researchers are beginning to trace the etiology of HF partly to
genetics
-The fundamental basis for heart cells are
-1) the generation of a contractile force,
- 2) transmission of this force throughout.
-Mutations in the sarcomere proteins of muscle cells have been
linked to HF. These mutations
- cause uncoordinated heart contractions  increased energy
consumption
- cause changes in calcium homeostasis  apoptosis and fiber
formation  inflammation
‫األسباب‬
‫‪(1‬‬
‫‪(2‬‬
‫‪(3‬‬
‫‪(4‬‬
‫‪(5‬‬
‫‪(6‬‬
‫‪(7‬‬
‫‪(8‬‬
‫أمراض الشرايين االكليلية‬
‫أمراض الصمامات‬
‫اعتالالت العضلة القلبية‬
‫ارتفاع التوتر الدموي الشرياني‬
‫األمراض الغدية(السكري‪,‬فرط أو قصور الدرق‪,‬تناذر‬
‫كوشينغ‪,‬ورم القواتم‪.).....‬‬
‫أمراض ارتشاحية(الساركوئيد‪,‬داء الصباغ الدموي‪,‬الداء‬
‫النشواني‪.)....‬‬
‫طبيعة الحياة(التدخين‪,‬الكحول‪,‬البدانة‪,‬نقص الفيتامينات‬
‫وخاصة‪)...B1‬‬
‫األدوية(مضادات األورام‪,‬حاصرات قنوات الكالسيوم‪,‬حاصرات‬
‫بيتا‪.)...‬‬
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
Adaptive mechanisms of the heart
to increased load
• Frank
- Starling mechanism
• Ventricular hypertrophy
– increased mass of contractile elements  strength
of contraction
• Increased
sympathetic adrenergic activity
– increased HR, increased contractility
• Incresed
activity of R–A–A system
General pathomechanisms involved in heart
failure development
Cardiac mechanical dysfunction can develop as
a consequence in preload, contractility and afterload
disorders
Disorders of preload
 preload  length of sarcomere is more than optimal 
  strength of contraction
 preload  length of sarcomere is well below the optimal 
  strength of contraction
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
2. Changes of neurohumoral control of the heart
function
• Physiology: • SNS   contractility
 HR
 activity of physiologic pacemakers
Mechanism:   sympathetic activity  cAMP 
Ca ++i  contractility
  sympathetic activity  influence
of parasympathetic system on the heart
• Pathophysiology: normal neurohumoral control is
changed and creation of pathologic
neurohumoral mechanisms are present
Chronic heart failure (CHF) is characterized by an imbalance of
neurohumoral adaptive mechanisms with a net results of excessive
vasoconstriction and salt and water retention
Catecholamines : - concentration in blood :
- norepinephrin – 2-3x higher at the rest than in healthy subjects
- circulating norepinephrin is increased much more
during equal load in patients suffering from CHF than
in healthy subject
-  number of beta 1 – adrenergic receptors 
 sensitivity of cardiomyocytes to catecholamines 
  contractility
System rennin – angiotensin – aldosteron
heart failure  CO  kidney perfusion  stim. Of RAA system
Important:
Catecholamines and system RAA = compensatory mechanisms
 heart function and arterial BP
The role of angiotensin II in development of heart
failure
 vasoconstriction ( in resistant vesels)
 retention of Na  blood volume
  releasing of arginin – vasopresin peptide (AVP )
from neurohypophysis
Main causes and pathomechanisms of diastolic
heart failure
1. structural disorders passive chamber stiffness
a) intramyocardial
– e.g. myocardial fibrosis, amyloidosis, hypertrophy,
myocardial ischemia...
b) extramyocardial – e.g. constrictive pericarditis
2. functional disorders   relaxation of chambers e. g. myocardial
ischemia, advanced hypertrophy of ventricles,
failing myocardium, asynchrony in heart
functions
Result of
Compensatory
Mechanisms >
Heart Failure
Heart Failure
Explained
Hypertension
• Hypertension — Data from the Framingham
Heart Study found that, after age 40, the lifetime
risk of developing HF was twice as high in
subjects with a blood pressure ≥160/100 mmHg
compared to <140/90 mmHg .
• Another analysis from the Framingham study
suggests that baseline systolic pressure and pulse
pressure have a greater impact on the risk of
subsequent HF than the diastolic pressure.
heart failure
outlines
– Definition
– Causes and pathophysiology
– Clinical manifestations
– Classification of heart failure
– Diagnostic evaluation
– Medical management
Definition of Heart Failure
Classification
I. Heart Failure with
Reduced Ejection Fraction
(HFrEF)
Ejection
Fraction
≤40%
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.
≥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.
II. Heart Failure with
Preserved Ejection
Fraction (HFpEF)
‫قصور القلب االنقباضي ‪ /‬االنبساطي‬
‫‪ ‬في القصور االنقباضي يكون االضطراب األساسي هو عدم القدرة على‬
‫ضخ دم كاف بسبب اضطراب القلوصية (التالي مثالً العتالل عضلة‬
‫القلب التوسعي أو االحتشاء) وهنا يتوسع البطين ويتمدد أثناء االنبساط ‪,‬‬
‫وبالتالي يزداد حجم نهاية االنبساط ‪ ,‬ولكن دون ازدياد مو في حجم‬
‫النفضة ‪.‬‬
‫‪ ‬أما في القصور االنبساطي فتضطرب قدرة البطين على االرتخاء جيدا ً‬
‫أثناء االنبساط ‪ ,‬لذا يضطرب الملء االنبساطي ويكون ضغط نهاية‬
‫االنبساط مرتفعا ً مهما كان حجم نهاية االنبساط ‪ ,‬وبمعنى آخر تكون‬
‫العالقة بين حجم النفضة وحجم نهاية االنبساط سوية (فالقلب يقذف جيدا ً‬
‫ما يحتوي من دم ولكن مشكلته هي في قلة ما يحتويه من هذا الدم ‪ ,‬عكس‬
‫القصور االنقباضي حيث يحتوي دما ً كثيرا ً ولكنه يعجز عن قذفه ) ‪.‬‬
‫ونرى القصور االنبساطي في اعتالل العضلة القلبية الضخامي مثالً ‪.‬‬
‫قصور القلب الحاد ‪ /‬المزمن‬
‫‪‬يظهر القصور الحاد مثالً في سياق أحتشاء واسع أو تمزق‬
‫صمامي مفاجئ ‪ ,‬فيقل النتاج القلبي ويهبط ضغط الدم الشرياني‬
‫دون حدوث وذمات محيطية‪.‬‬
‫‪‬القلب المزمن يكون ضغط الدم سويا ً ( بسبب نشاط آليات‬
‫المعاوضة كضخامة عضلة القلب ونشاط الجهاز الودي وازدياد‬
‫الكاتيوكول آمينات ) ‪ ,‬لكن تحدث الوذمات المحيطة نتيجة‬
‫تراكم السوائل في األنسجة الخاللية‪.‬‬
‫قصور أيسر القلب ‪ /‬أيمن القلب‬
‫‪‬في قصور أيسر القلب التالي لضعف في عضلة القلب كاالحتشاء‬
‫أو كالتضيق األبهري ‪ ,‬تتراكم السوائل ويرتفع الضغط خلف‬
‫البطين األيسر نتيجة ضعف الضخ ‪ ,‬فيرتفع الضغط في األوردة‬
‫الرئوية وفي األوعية الشعرية الرئوية وتظهر أعراض االحتقان‬
‫الرئوي ‪.‬‬
‫‪‬أما في قصور القلب األيمن فتتراكم السوائل خلف البطين األيمن ‪,‬‬
‫فتظهر الوذمات المحيطة وضخامة الكبد االحتقانية والتوسع‬
‫الوريدي الجهازي ‪.‬‬
‫‪‬مالحظة ‪ :‬تكون الحدود بين هذين الشكلين أقل وضوحا ً في‬
‫الحاالت المزمنة ‪.‬‬
‫قصور القلب عالي النتاج ‪ /‬منخفض النتاج‬
‫‪‬يحدث القصور عالي النتاج مشاركا ً لفرط الدرقية وفقر الدم الشديد‬
‫و النواسير الشريانية الوريدية وداء باجت ‪ ...‬ألنه على القلب أن‬
‫يضخ كميات كبيرة من الدم لكي يوصل األوكسجين بكميات كافية‬
‫الحتياجات النسج التي لديها زيادة في االستقالب ‪.‬لذا تكون‬
‫األطراف دافئة وضغط النبض واسعا ً ( أو على األقل سويا ً )‪.‬‬
‫‪ ‬على عكس القصور منخفض النتاج حيث يحدث تقبض وعائي‬
‫محيطي ‪ ,‬وتكون األطراف باردة شاحبة وأحيانا ً مزرقة ‪ ,‬وفي‬
‫الحاالت المتقدمة يصبح ضغط النبض صغيرا ً بسبب حجم النفضة‬
‫‪.‬‬
‫قصور القلب اإلقبالي ‪Forward -‬‬
‫اإلدباري ‪Backward‬‬
‫‪‬و هذا التفريق لتمييز اآلليات المحدثة الحتباس السوائل و‬
‫الوذمات ‪ .‬حيث يقول مؤيدو نظرية القصور اإلدباري إنه عند‬
‫حدوث القصور يفشل البطين في ضخ محتوياته و لذا ترتفع‬
‫الضغوط خلفه و يحدث احتباس للماء و الصوديوم كنتيجة‬
‫الرتفاع الضغوط الشعرية و الوريدية و ارتشاح السوائل إلى‬
‫المسافات الخاللية ‪.‬‬
‫‪‬أما أصحاب نظرية القصور اإلقبالي فيدعون أن قصور القلب‬
‫في ضخ الدم إلى الشرايين الجهازية يؤدي إلى إقفار كلوي و‬
‫ازدياد عودة امتصاص الصوديوم في النبيبات القريبة كنتيجة‬
‫لتحريض جهاز الرينين – ألدسترون و بذلك يحدث احتباس‬
‫الماء و الملح ‪.‬‬
‫تصنيف قصور القلب وفقا لمراحل الزلة التنفسية‬
‫‪NYHA‬تبعا للجمعية األمريكية ألمراض القلب‬
‫‪class‬‬
‫‪I‬‬
‫‪II‬‬
‫‪III‬‬
‫‪IV‬‬
‫الزلة التنفسية‬
‫تحدث عند الجهد الشديد‬
‫تحدث عند الجهود المتوسطة كاألعمال المنزلية‬
‫تحدث عند الجهود الخفيفة‬
‫تحدث على الراحة‬
Ischemic cardiomyopathy
• Ischemic cardiomyopathy is diagnosed in
patients with HF who have had a myocardial
infarction or have evidence of hibernating
myocardium or, on angiography, severe
coronary disease.
• In contrast, patients with single vessel disease
who have no evidence of myocardial infarction
or revascularization have a similar prognosis
as those with nonischemic cardiomyopathy .
‫‪A‬‬
‫‪STAGE‬‬
‫‪‬تشمل المرضى الذين لديهم عوامل خطورة لتطور‬
‫قصور القلب(المسنين‪,‬السكري‪,‬ارتفع الضغط‬
‫الشرياني‪,‬ارتفاع الكوليسترول‪,‬التدخين‪,)......‬وهؤالء‬
‫المرضى ليس لديهم أي أعراض أو عالمات أو‬
‫اضطراب في بنية العضلة القلبية‪.‬‬
‫‪‬جميع هؤالء المرضى يجب أن يخضعوا للعالج‬
‫الدوائي لمنع التطور للمرحلة التالية‬
‫‪B‬‬
‫‪STAGE‬‬
‫‪‬هم المرضى الذين تطور لديهم خلل في بنية‬
‫العضلة القلبة لكنهم ما زالوا ال يعانون من أي‬
‫أعراض أو عالمات لقصور القلب‪.‬‬
‫‪STAGE C‬‬
‫‪‬هم المرضى الذين تطور لديهم أعراض‬
‫قصور القلب باالضافة لوجود الخلل في بنية‬
‫العضلة القلبية‪.‬‬
‫‪D‬‬
‫‪STAGE‬‬
‫‪‬هي مرحلة متطورة من قصور القلب‬
‫حتى أن معظم العالجات المستخدمة لم‬
‫تعد تفيد‪.‬‬
‫‪%50‬من هؤالء المرضى يموتون خالل‬
‫‪6‬أشهر وهم يقابلون المرحلة ‪ IV‬من‬
‫تصنيف ‪.NYHA‬‬
Sensitivity, Specificity, and Predictive Accuracy of Symptoms and Signs for Diagnosing
Heart Failure
Modified Framingham clinical criteria
for the diagnosis of heart failure
Major
• Paroxysmal nocturnal dyspnea
• Orthopnea
• Elevated jugular venous pressure
• Pulmonary rales
• Third heart sound
• Cardiomegaly on chest x-ray
• Pulmonary edema on chest x-ray
• Weight loss ≥4.5 kg in five days in response to
treatment of presumed heart failure
Framingham criteria - c
•
•
•
•
•
•
•
•
Minor
Bilateral leg edema
Nocturnal cough
Dyspnea on ordinary exertion
Hepatomegaly
Pleural effusion
Tachycardia (heart rate ≥120 beats/min)
Weight loss ≥4.5 kg in five days
question
• 1. A 75 year-old male presents to you with a gradual onset of
symptoms suggestive of heart failure and sinus rhythm and
examination confirms the presence of biventricular failure.
Following confirmation of the diagnosis by chest x-ray and
electrocardiography you should take the following steps:
a. Treat the heart failure with diuretics and ACE inhibitors .
b. Treat the heart failure with digoxin and diuretics.
c. Treat he patient with diuretics, ACE inhibitors and
anticoagulants .
d. Try to establish the cause of the heart failure with
echocardiography, cardiac catheterisation and whatever other
investigations are appropriate .
e. Use ACE inhibitor, vasodilator therapy and diuretic .
CLINICAL Evaluation
• The approach to the patient with suspected HF
includes the FOLLOWING :
• history
• physical examination
• diagnostic tests to help establish the diagnosis
• assess acuity and severity
• initiate assessment of etiology.
History and Physical Examination
I IIaIIbIII
I IIaIIbIII
I IIaIIbIII
A thorough history and physical examination should be
obtained/performed in patients presenting with HF to
identify cardiac and noncardiac disorders or behaviors
that might cause or accelerate the development or
progression of HF.
In patients with idiopathic DCM, a 3-generational family
history should be obtained to aid in establishing the
diagnosis of familial DCM.
Volume status and vital signs should be assessed at
each patient encounter. This includes serial assessment
of weight, as well as estimates of jugular venous
pressure and the presence of peripheral edema or
orthopnea.
History
• Classic exertional angina usually indicates
ischemic heart disease.
• Acute HF after an antecedent flu-like illness
suggests viral myocarditis.
.
• Long-standing hypertension or alcohol use
suggests hypertensive or alcoholic
cardiomyopathy.
• Primary valvular dysfunction should be
considered in a patient with a history of
murmurs.
HISTORY -C
• a family history of unexplained cardiomyopathy, low
voltage on EKG, left ventricular hypertrophy (especially
without hypertension),and a history of heavy proteinuria.
• A diagnosis of amyloidosis should be strongly considered
• HF may be provoked or worsened by drugs, including
antiarrhythmic agents such as disopyramide and flecainide ;
calcium channel blockers, particularly verapamil ; beta
blockers; and nonsteroidal antiinflammatory drugs
(NSAIDs) .
• (Acute pulmonary edema occurring during, or shortly after,
infusion of blood products suggests transfusional volume
overload.
Vital signs and appearance
• Four major findings suggest severity of the cardiac
dysfunction:
• resting sinus tachycardia, narrow pulse pressure,
diaphoresis, and peripheral vasoconstriction.
• A decrease in cardiac output should be suspected when
the pulse pressure is reduced below 25 mmHg.
• Pulsus alternans, if present, is virtually pathognomonic of
severe left ventricular failure.
Volume assessment
• There are three major manifestations of
volume overload in patients with HF:
• pulmonary congestion,
• peripheral edema,
• and elevated jugular venous pressure.
Diagnostic Tests
I IIaIIbIII
A 12-lead ECG should be performed initially on all patients
presenting with HF.
I IIaIIbIII
I IIaIIbIII
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.
Electrocardiogram
• prior or acute myocardial infarction or ischemia.
• Left ventricular hypertrophy due to hypertension.
• Low limb lead voltage on the surface ECG with a pseudo-infarction pattern
(loss of precordial R wave progression in leads V1-V6) can suggest an
infiltrative process such as amyloidosis.
• Low limb lead voltage with precordial criteria for left ventricular
hypertrophy is most suggestive of idiopathic dilated cardiomyopathy. A
widened QRS complex and/or a left bundle branch block pattern is also
consistent with this diagnosis.
• Heart block, that may be complete, and various types of intraventricular
conduction defects are observed in patients with cardiac sarcoidosis.
• The presence of a persistent tachycardia such as atrial fibrillation with a
rapid ventricular response may result from or lead to HF, since this
arrhythmia can cause cardiomyopathy (tachycardia-mediated
cardiomyopathy).
Noninvasive Cardiac Imaging
I IIaIIbIII
Patients with suspected or new-onset HF, or those presenting with acute
decompensated HF, should undergo a chest x-ray to assess heart size and
pulmonary congestion, and to detect alternative cardiac, pulmonary, and other
diseases that may cause or contribute to the patients’ symptoms.
I IIaIIbIII
A 2-dimensional echocardiogram with Doppler should be performed during initial
evaluation of patients presenting with HF to assess ventricular function, size, wall
thickness, wall motion, and valve function.
I IIaIIbIII
Repeat measurement of EF and measurement of the severity of structural
remodeling are useful to provide information in patients with HF who have had a
significant change in clinical status; who have experienced or recovered from a
clinical event; or who have received treatment, including GDMT, that might have
had a significant effect on cardiac function; or who may be candidates for device
therapy.
Chest x-ray
• cardiomegaly (cardiac-to-thoracic width ratio
above 50 percent)
• cephalization of the pulmonary vessels
• Kerley B-lines, and pleural effusions .
• The cardiac size and silhouette may also reveal
signs of congenital anomalies (ventricular or
atrial septal defect) or valvular disease (mitral
stenosis or aortic stenosis).
‫الموجودات على صورة الصدر الشعاعية‬
‫‪CX-RAY‬‬
‫‪‬زيادة المشعر القلبي الصدري‪.‬‬
‫‪‬زيادة االحتقان الرئوي على شكل وذمة‬
‫خاللية(خطوط كيرلي)أو وذمة سنخية(منظر‬
‫جناحي الخفاش)‪.‬‬
‫‪‬اعادة توزع األوعية لألعلى‪.‬‬
‫‪‬انصباب جنب‪.‬‬
This plain frontal radiograph of the chest in a 51year-old male demonstrates marked enlargement
of the cardiac silhouette compatible with a dilated
cardiomyopathy. Cardiomegaly is nonspecific and
can be seen with any etiology of cardiomyopathy.
ECHOCARDIOGRAPHY
• Atrial and ventricular sizes,
• Global left and right ventricular systolic function (left and
right ventricular ejection fraction, LVEF and RVEF).
• Diastolic left ventricular function.
• Regional wall motion abnormalities in a coronary
distribution are suggestive of coronary heart disease but
segmental abnormalities also occur commonly in patients
with dilated cardiomyopathy
• Pericardial disease includes thickening suggestive of
constrictive pericarditis or effusion which may or may not
be associated with tamponade.
• Valvular heart disease
Diagnostic Tests
I IIaIIbIII
I IIaIIbIII
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.
Initial blood tests
• A complete blood count which may suggest concurrent or alternate
conditions. Anemia or infection can exacerbate preexisting HF.
• Serum electrolytes, blood urea nitrogen and creatinine may indicate
associated conditions.
• Hyponatremia generally indicates severe HF, though it may
occasionally result from excessive diuresis .
• Renal impairment may be caused by and/or contribute to HF
exacerbation. Baseline evaluation of electrolytes and creatine is also
necessary when initiating therapy with diuretics and/or angiotensin
converting enzyme inhibitors.
• Liver function tests, which may be affected by hepatic congestion.
• Fasting blood glucose to detect underlying diabetes mellitus.
Additional tests
• Thyroid function tests, particularly in patients over the
age of 65 or in patients with atrial fibrillation.
Thyrotoxicosis is associated with atrial fibrillation and
hypothyroidism may present as HF.
• Iron studies (ferritin and TIBC) to screen for hereditary
hemochromatosis (HH). In the past, prior to increased
screening, cardiac disease was the presenting
manifestation in up to 15 percent of patients with HH.
Thus, the absence of other characteristic findings of HH
does not preclude the diagnosis.
‫‪BNP‬الببتيد المدر للصوديوم‬
‫• يفرز من قبل البطين كاستجابة للشد على جدره ‪ ,‬بسبب‬
‫ارتفاع الضغط داخل أجواف القلب‪ ,‬في مرضى استرخاء‬
‫القلب االحتقاني ‪.‬‬
‫• يتناسب مستوى ارتفاع ‪ , plasma BNP levels‬تبعا‬
‫للضغط في نهاية االنبساط‪.‬‬
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 (cont.)
I IIaIIbIII
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.
I IIaIIbIII
The usefulness of serial measurement of BNP or NT-proBNP to
reduce hospitalization or mortality in patients with HF is not
well established.
I IIaIIbIII
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.
Hospitalized/Acute
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.
I IIaIIbIII
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
The usefulness of BNP- or NT-proBNP guided therapy for
acutely decompensated HF is not well-established.
I IIaIIbIII
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.
‫الموجودات المخبرية‬
‫‪‬قد تكون طبيعية أو تدل على وجود مرض معين (فقر‬
‫الدم‪,‬فرط الدرق‪,‬ارتفاع أو هبوط الكالسيوم أو البوتاسيوم‪).....‬‬
‫‪‬الببتيد الطارح للصوديوم‪ BNP‬مستواه من ‪ 400-100‬فاذا‬
‫كان ‪:‬‬
‫‪ 100<BNP ‬تشخيص السبب القلبي غير محتمل‬
‫‪400-100=BNP‬التشخيص غير أكيد‬
‫‪400>BNP ‬يوجد اضطراب بنيوي في عضلة القلب ‪.‬‬
‫القيم التشخيصية‬
• BNP level below 100 pg per milliliter
indicates that heart failure is unlikely
• BNP level greater than 500 pg per milliliter
indicates heart failure
• BNP levels between 100 and 500 pg per
milliliter provide inadequate diagnostic
discrimination.
Causes for Elevated Natriuretic Peptide
Levels
Cardiac
 Heart failure, including RV
syndromes
 Acute coronary syndrome
 Heart muscle disease, including
LVH
 Valvular heart disease
 Pericardial disease
 Atrial fibrillation
 Myocarditis
 Cardiac surgery
 Cardioversion
Noncardiac
 Advancing age
 Anemia
 Renal failure
 Pulmonary causes: obstructive
sleep apnea, severe pneumonia,
pulmonary hypertension
 Critical illness
 Bacterial sepsis
 Severe burns
 Toxic-metabolic insults, including
cancer chemotherapy and
envenomation
Noninvasive Cardiac Imaging (cont.)
I IIaIIbIII
Magnetic resonance imaging is reasonable when
assessing myocardial infiltrative processes or scar
burden.
I IIaIIbIII
No Benefit
Routine repeat measurement of LV function
assessment in the absence of clinical status change or
treatment interventions should not be performed.
Invasive Evaluation (cont.)
I IIaIIbIII
When ischemia may be contributing to HF, coronary
arteriography is reasonable for patients eligible for
revascularization.
I IIaIIbIII
Endomyocardial biopsy can be useful in patients presenting with
HF when a specific diagnosis is suspected that would influence
therapy.
EXERCISE TESTING
• Exercise testing should be part of the initial
evaluation of any patient with HF. In addition to
detection of ischemic heart disease, assessment
of exercise capacity can be used for risk
stratification and determining prognosis; serial
measurements also can assess the efficacy of
therapy and clinical stability of patients over
time.
• A simple alternative that provides an estimate of
exercise function is the six minute walk test.
‫مؤشرات الموت في مرضى استرخاء القلب‬
‫•‬
‫•‬
‫•‬
‫•‬
‫•‬
‫نقص ‪ Na‬الدم‬
‫عرض ‪QRS‬‬
‫ارتفاع مستوى النورابينفرين‬
‫نقص ‪LV EF %‬‬
‫ارتفاع ‪BNP‬‬
SUMMARY AND RECOMMENDATIONS
• Initial evaluation of patients with symptoms or
signs suggestive of heart failure (HF) includes
clinical assessment (history and physical exam),
electrocardiogram, blood tests, and chest x-ray.
• Early measurement of plasma BNP or NT proBNP levels is suggested in patients with suspected
HF in whom the diagnosis is uncertain.
• In patients with symptoms and signs of HF,
echocardiography is useful for evaluating
hemodynamics and identifying potential causes of
HF.