Scribd
Upload
49 views

Continue of The Signs of Heart Failure:-: Most Patent With HF Are Hypotensive Due To Poor

This document summarizes signs and symptoms of heart failure and methods for diagnosis and management. Key signs include pale skin, elevated jugular venous pressure, shifted apex beat location, heart sounds like S3 gallop or murmurs, hepatomegaly, leg edema, and ascites. Diagnosis involves ECG, chest X-ray, echocardiogram, BNP levels, and other tests. Management focuses on decreasing preload and afterload via diuretics like furosemide to relieve symptoms, while also preventing heart remodeling through additional treatments.

Uploaded by

AbdulJabar Riadh
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd
49 views

Continue of The Signs of Heart Failure:-: Most Patent With HF Are Hypotensive Due To Poor

This document summarizes signs and symptoms of heart failure and methods for diagnosis and management. Key signs include pale skin, elevated jugular venous pressure, shifted apex beat location, heart sounds like S3 gallop or murmurs, hepatomegaly, leg edema, and ascites. Diagnosis involves ECG, chest X-ray, echocardiogram, BNP levels, and other tests. Management focuses on decreasing preload and afterload via diuretics like furosemide to relieve symptoms, while also preventing heart remodeling through additional treatments.

Uploaded by

AbdulJabar Riadh
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd
You are on page 1/ 8

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 !

You might also like