Continue of the signs of heart failure :-

5- Pale skin due to high sympathetic tone

6- most patent with HF are hypotensive due to poor
contractility of the LV while in diastolic LV dysfunction most of
them are Hypertensive

7- by the examination of jagular venous pressure the patient

usually have raised JVP and if you see prominent B wave this
mean the patient have tricuspid regugetation , and if you see
absence of the A wave this mean the patient had atrial
fibrillation

8- Regarding to the precordium :

The apex beat usually shift just lateral to the mid calvicular line
 LV dalitation

 If the patient have Left parasternal heave  pulmonary

hypertension

9- Auscultation :
 You may hear faint S1+S2 heart sound or may hear S3 gallop
rhythm or might hear summation gallop (just like running
horse) or might hear a murmur indicating mitral or tricuspid
regurgitation or some times aortic valve regurgitation [ due
dalitaion of the valve ]
 If you auscultalte the base of the lung you might hear 
crackles or criptations [ like moving fluid during inspiration
and expiration ] , character of these crackles is don’t
disappear with cough
 ‫ يعني لمن نسمع هذا الصوت نطلب من المريض ان يكح فاذا اختفى الصوت‬
‫معناها المشكلة بالجهاز التنفسي مثل عدوى او شي ثاني اما اذا بقى الصوت‬
‫معناتها السبب هوه عجز القلب‬

10- by the examination of the abdomen you might find tender

Hepatomegaly or sometimes the liver looks like pulsating liver ,
presence of these indicating the patient have tricuspid valve
regurgitation

And in advanced heart failure you may find free fluid in

abdominal cavity thats called  Ascites

11- by the examination of the legs you may fine  Bilateral leg
edema , Sacral edema

+ In advanced heart failure may found  Scrotal edema in

males.
 Diagnosis of heart failure
A- specific :
1- ECG :-
For the diagnosis of underlying ischemic heart disease
For estimation the size of the champers
Detect of predict arrhythmia [ for detecting if this heart
arrhythmogenic or not ] ( because the cause of death in
patient with HF is sudden cardiac death ! )
Absence of sinus arrhythmia  high risk for sudden cardiac
death
Absence of RR interval variability  high risk for sudden
cardiac death
The longer QT interval  More risk for arrhythmia
T wave desperation  more liable for arrhythmia + sudden
cardiac death
For predicting arrhythmia of the heart :-
 ECG  detect RR interval variability
 QT interval
 T – wave desperation
 24 – hour hulter monitoring
 Signal average ECG : to detect the late potential in the
heart (the pt with late potential is liable for arrhythmia )
2- Chest X-ray :-
for diagnosis of champer size and any evidence of pulmonary
congestion and pulmonary hypertrension
the patient can have cardiomegaly in spite of normal cardio-
thoracic ratio (which is < 50% ) by comparism with previous
chest x-ray !
Heart failure can cause Right sided plural effusion or in
advanced case it cause Bilateral plural effusion But it NEVER
EVER cause Left sided plural effusion !
Kerley B lines is horizontal parallel lines situated on both
sides of the lung on chest X-ray indicating pulmonary
congestion

3- Echocardiography :-
Which can estimate cardiac champer size , ejection fraction ,
stroke volume , cardiac output , any defective valvular
function and currently we can predict the
arrhythemogenicity of the heart , etc ...

4- Blood tests :-
a- brain natriuretic peptide : indicating that the patient
have LV dalitation  heart failure

- This test used to differentiate between sever brochial

asthma and acute pulmonary edema ( acute HF ) , so if
the test (+)  heart failure
- And if the test (-)  respiratory problem
  Pulmonary function test in HF the test Restrictive while in
respiratory diseases it can be Restrictive or Obstructive
B- atrial natriuretic peptide.

5- CT-angiography
6- ECG gated MRI
7- Cardiac catheterization

B- General(Non specific) :-
1- Thyroid function test

2- Random blood sugar : diabetes ...

3- HB and PCV : because sometimes polycythemia and

hemosedrosis might induce heart failure

4- Lipid profile : Hyperlipidemia ...

5- Renal function test : because most of the patient have
Cardio-renal syndrome

 Normal urea < 40 mg/dl

 Normal creatinin < 1 mg/dl
6- Liver function test : for case of hepatic congestion and
liver dysfunction

7- Electrolyte ( Na, K , Ca , Mg ) : any disruption of these

indicating the patient liable for arrhythmia and sudden cardiac
death .

Tests of the viability of the myocardium :

Echo stress test , ECG gated MRI , PET- scan , Thalium stress
test .
 Management
treatment in patient with heart failure is focused
at the following )‫ (الخطة العالجية‬:-
1-decrease the symptoms of the patient
2-to prevent the remodelling
3- to prevent complication
 to relive the symptoms by decreasing the preload
and decreasing the afterload and increase the
intrinsic activity of the heart .

1- Diuretics :- For decreasing the preload (heart

failure patient without diuretics cannot survive !! )
and we use at first loop diuretics
 Starting treatment with injectable diuretics to
relive the congestion and then continuo as oral
treatment
 Loop diuretics [ Ferusemide , toresemide ]
 Furosemide causes excretion of water , Na , K . so
it cause Hyponatremia , hypokalemia ,
hyperglycemia , hyperurecemia , hypocalcemia ,
hypomagnesemia .
  Diuretics cause dramatic response and improve the
symptoms but it not improve the 5-years survival
because it don’t attack remodelling

 Toresemide is same as furosemide but it differ by

the following :
 Its more safe when the patient have renal
impairment
 It cause less sever hypokalemia
 It has anti-fibrotic effect [anti-remodilling
effect ]
 The diuretics have whats called [ preconditioning ]
phenomenon which resembling Tachyphylaxis (
decrease in body response to the drug ) and to
prevent this we do the following :-
 Give the patient changeable dose Not fix dose of
diuretics [‫]مثال حبه الصبح و حبايتين الظهر وحبه بالليل‬
 Or give two diuretics at the same time [ex:
feurosemid+thiazide...]
 Also the diuretics have rebound absorbition of the Na
( Which occur after sudden abrupt of the drug )
 But at long-term use of diuretic it will cause
progressive decrease of renal blood flow  activation
of rennin-angiotensin system  More remodelling
effect !