1 Magdi Awad Sasi Heart Failure 2013

Heart Failure
MAGDI AWAD SASI 2013
1 MAGDI AWAD SASI HEART FAILURE 2013

DEFINITION
Heart (or cardiac) failure: pathophysiological state in
which the heart is unable to pump blood at a rate
commensurate with the requirements of the
metabolizing tissues or can do so only from an
elevated filling pressure
According to AHA,
HF is a clinical syndrome including circulatory

congestion or inadequate tissue perfusion , due to
abnormal heart function and associated
neurohormonal abnormalities.
An inadequate or decreased cardiac output which

causes an increase in the blood volume within the
vascular system. The resulting congestion within the
venous system interferes with the movement of body
fluids, resulting in fluid accumulation in the tissue
spaces, causing edema
Frequency : United States

More than 3 million people have congestive heart
failure (CHF), and more than 400,000 new patients
present yearly. The prevalence rate is 1-2%.
Race
Blacks are 1.5 times more likely to die of CHF than

whites are. Nevertheless, black patients appear to
have similar or lower in-hospital mortality rates than
white patients.
Sex
Prevalence is greater in males than in females in

patients aged 40-75 yrs.

No sex predilection is noted among patients older
than 75 years.
Age
Prevalence of CHF increases with increasing age and

affects about 10% of the population older than 75
years
Mortality/Morbidity
Approximately 30-40% of patients with congestive

heart failure (CHF) are hospitalized every year. CHF is
the leading diagnosis-related group (DRG) among
hospitalized patients older than 65 years. 35% will
die within one year of diagnosis. Less than 50% of
patients with HF have typical physical signs. Less
than 50% of patients being correctly identified during
the initial consultation. 50% readmission rate within 6
months
50% of HF patients will die 5 years after the

diagnosis
The most common cause of death is progressive heart

failure, but sudden death may account for up to 45%
of all deaths.
Patients with coexisting insulin-dependent diabetes

mellitus have a significantly increased mortality rate .

Cardiac Physiology
(remember this?)
CO = SV x HR
HR: parasympathetic
and sympathetic tone
SV: preload, afterload,
contractility
Preload
Def: Passive stretch of
muscle prior to contraction
Measurement: Swan-Ganz
LVEDP( venous return)
Really a function of diastole
Affected by compliance
Low compliance = higher LVEDP with lower
LVEDV
Afterload
Def: Force opposing/stretching muscle after
contraction begins
Measurement: SVR
Contractility

Def: Normal ability of the muscle to contract at
a given force for a given stretch, independent
of preload or afterload forces
In other words:
How healthy is your heart muscle?
Ischemia,infarction, Hypertrophy (?), Muscle
loss
Pathophysiology
Hemodynamic changes
Neurohormonal changes
Cellular changes
1.Hemodynamic changes:
HF can be secondary to systolic dysfunction or
diastolic dysfunction
2. Cellular changes
Changes in Ca+2 handling
Changes in adrenergic receptors:
Slight in 1 receptors
1 receptors desensitization followed by down
regulation
Changes in contractile proteins
Program cell death (Apoptosis)
Increase amount of fibrous tissue
3. Neurohormonal changes

Classifying Heart Failure
Forward Vs Backward
Rt. Vs Lt. sided HF
Acute Vs Chronic HF
Low Vs High output HF
Systolic Vs Diastolic HF

A etiology It is a common end point for many diseases
of cardiovascular system
1. Vascular
Ischemic heart
disease,
myocardial
infarction
2. Valvular
stenosis/regurgitation( RHD, infective endocarditis)
3. Preesure- hypertension
4.Muscle- cardiomyopathy
5. Rhythm- atrial fibrillation
Symptoms:
Left ventricular failure-
The patient present with chest symptoms which may delay

the diagnosis and keep the patient to seek chest
consultants advice.
Failure of forward flow from left ventricle into the aorta

result into pulmonary congestion with chest symptoms.

Since the left ventricle does not empty completely, it
cannot accept blood returning from the lungs via the
pulmonary veins. The pulmonary veins become engorged
and fluid seeps out through the veins and collects in the
lungs.
LVF can be acute or chronic depending on the underlying

cause of heart disease
LVF= CHEST SYMTOMS= D/D OF ALL LUNG DISEASES=

CHEST FINDING
LVF symptoms are:
Dyspnea at rest
Dyspnea upon exertion: This has been found to be the

most sensitive symptom reported, yet the specificity
for dyspnea is less than 60%.
Orthopnea and paroxysmal nocturnal dyspnea (PND):

These symptoms are observed; however, the
sensitivity for orthopnea and PND is only 20-30%.
Cough: Cough that produces pink, frothy sputum is

highly suggestive of congestive heart failure
(CHF).The sputum is whitish , soap like , watery.
Wheezing= new onset of wheezing above age of 60

years or wheezing in elder diabetic or wheezing all of
a sudden in HTN patient is cardiac asthma until prove
other wise.
Palpitation in arrhythmia
Chest pain or tightness especially if the cause is

vascular(IHD/ACS).
Non specific symptoms of low COP

Malaise, Weakness,Light headedness, fatigue, dizziness
,sweating ,lose of effort.

Right ventricular heart failure
The patient present with abdominal symptoms which may

delay the diagnosis and keep the patient to seek
gastroenterologist advice.
Failure of forward flow from right ventricle into the

pulmonary artery results into systemic congestion with
abdominal symptoms.
Failure of the right ventricle to maintain a normal output

of blood.
Since the right ventricle does not empty completely, it

cannot fully accept blood returning from the body.
Pressure builds in the veins of the body causing fluid to
seep out and collect in the cells of the body especially

the extremities. Engorgement of the systemic veins
produces pitting edema, enlargement of the liver, and
ascites.
RVF can be acute or chronic depending on the underlying

cause of heart disease
RVF= ABDOMENAL SYMTOMS= D/DOF ABDOMENAL

DISEASES= ABD FINDING.
Right-sided or right ventricular (RV) heart failure usually

occurs as a result of left-sided failure. When the left
ventricle fails, increased fluid pressure is, in effect,
transferred back through the lungs, ultimately damaging
the heart's right side. When the right side loses pumping
power, blood backs up in the body's veins. This usually
causes swelling in the legs and ankles.
RVF symptoms are:
Abdominal distention
Right hypochondrial pain
Epigastric fullness, early satiety , nausea ,
vomiting(stomach congestion)
Change of bowel habit constipation, diarrhea,
malabsorption
Bilateral leg swelling
Yellowish coloration of sclera
Change of urine frequency and colour
These symptoms are caused by internal abdominal

organs congestion
And can be mistaken for local abdominal pathology.
RVF is caused by:

1. Left ventricular failure - most common cause- mitral
stenosis
2. Pulmonary hypertension caused by chronic lung

disease
(cor
pulmonale)
3. Cardimyopathies and
myocarditis
SIGNS:
General appearance
Patients with mild heart failure appear to be in

no distress after a few minutes of rest, but they
may be obviously dyspneic during and
immediately after moderate activity. Patients
with LV failure may be dyspneic when lying flat
without elevation of the head for more than a
few minutes. Those with severe heart failure
appear anxious and may exhibit signs of air
hunger in this position.
Patients with recent onset of heart failure are

generally well nourished, but those with chronic
severe heart failure are often malnourished and
sometimes even cachectic.
Chronic marked elevation of systemic venous

pressure may produce exophthalmos and severe
tricuspid regurgitation and may lead to visible
pulsation of the eyes and of the neck veins.

Central cyanosis, icterus, and malar flush may be
evident in patients with severe heart failure.
In mild or moderate heart failure, stroke volume

is normal at rest; in severe heart failure, it is
reduced, as reflected by a diminished pulse
pressure and a dusky discoloration of the skin.
With very severe heart failure, particularly if

cardiac output has declined acutely, systolic
arterial pressure may be reduced. The pulse may
be weak, rapid, and thready; the proportional
pulse pressure (pulse pressure/systolic pressure)
may be markedly reduced. The proportional pulse
pressure correlates reasonably well with cardiac
output.
Evidence of increased adrenergic activity
Increased adrenergic activity is manifested by

tachycardia, diaphoresis, pallor, peripheral
cyanosis with pallor and coldness of the
extremities, and obvious distention of the
peripheral veins secondary to venoconstriction.
Diastolic arterial pressure may be slightly

elevated.
Pulmonary rales =LVF
Rales heard over the lung bases( bilateral basal

end inspiratory) are characteristic of heart
failure of at least moderate severity.
The absence of rales certainly does not exclude

elevation of pulmonary capillary pressure due to
LV failure.

Protodiastolic (S3) gallop: This is the earliest cardiac
physical finding in decompensated heart failure in the
absence of severe mitral or tricuspid regurgitation or
left-to-right shunts.
LVF=CHEST-B/L BASAL INSPIRATORY CREPITATION +

HEART-S3
Systemic venous hypertension: This is manifested by

jugular venous distention. Normally, jugular venous
pressure declines with respiration; however, it
increases in patients with heart failure, a finding
known as the Kussmaul sign. This reflects an increase
in right atrial pressure and therefore right-sided
heart failure.
Hepatojugular reflux: This represents distension of

the jugular vein induced by applying manual pressure
over the liver. The patient's body should be positioned
at a 45 angle. This is found in patients with elevated
left-sided filling pressures and reflects elevated
capillary wedge pressure and left-sided heart failure.
Edema
Bilateral pitting pedal odema.
Usually, a substantial gain of extracellular fluid

volume (ie, a minimum of 5 L in adults) must
occur before peripheral edema is manifested.
Edema, in the absence of dyspnea or other signs

of LV or RV failure, is not solely indicative of
heart failure and can be observed in many other
conditions, including chronic venous
insufficiency, nephrotic syndrome, or other
syndromes of hypoproteinemia or osmotic
imbalance.

Hepatomegaly
Hepatomegaly is prominent in patients with

chronic right-sided heart failure, but it may occur
rapidly in acute heart failure.
When occurring acutely, the liver is usually

tender.
In patients with considerable tricuspid

regurgitation, a prominent systolic pulsation of
the liver, attributable to an enlarged right atrial V
wave, is often noted. A presystolic pulsation of
the liver, attributable to an enlarged right atrial A
wave, can occur in tricuspid stenosis, constrictive
pericarditis, restrictive cardiomyopathy involving
the RV, and pulmonary hypertension (primary or
secondary).
Hydrothorax (pleural effusion)
Hydrothorax is most commonly observed in

patients with hypertension involving both
systemic and pulmonary systems. Hydrothorax is
usually bilateral, although when unilateral, it is
usually confined to the right side of the chest.
When hydrothorax develops, dyspnea usually

intensifies because of further reductions in vital
capacity.
Ascites
This finding occurs in patients with increased

pressure in the hepatic veins and in the veins
draining into the peritoneum.

Ascites usually reflects long-standing systemic
venous hypertension.
Pulsus alternans ( one strong and one weak beat)
Pulsus alternans occurs most commonly in heart

failure due to increased resistance to LV ejection, as
occurs in hypertension, aortic stenosis, coronary
atherosclerosis, and dilated cardiomyopathy.
It is usually associated with an S3 gallop, signifies

advanced myocardial disease, and often disappears
with treatment of heart failure.
Accentuation of P2 heart sound, S3 gallop, and systolic

murmurs
This accentuation is a cardinal sign of increased

pulmonary artery pressure. It disappears or
improves after treatment of heart failure.
Mitral and tricuspid regurgitation murmurs are

often present in patients with decompensated
heart failure because of ventricular dilatation.
These murmurs often disappear or diminish when
compensation is restored. Note that correlation
between the intensity of the murmur of mitral
regurgitation and its significance in patients with
heart failure is poor. Severe mitral regurgitation
may be accompanied by soft murmur.
The presence of an S3 gallop in adults is

important, pathologic, and often the most
apparent finding on cardiac auscultation in
patients with significant heart failure.
Cardiac cachexia

Cardiac cachexia is found in long-standing heart
failure, particularly of the RV, because of
anorexia from hepatic and intestinal congestion
and sometimes because of digitalis toxicity.
Occasionally, impaired intestinal absorption of fat
and (rarely) protein-losing enteropathy occur.

Precipitating Factors
Infection Sodium Intake
Medications!!! Anemia
Thyroid disorders Endocarditis
Pulm Embolus Noncompliance
Arrhythmia Myocardial Infarction
Stress reaction
Diagnosis of CHF / Routine Tests:
CBC count INVESIVE

Electrolytes 1. Exercise stress test

Renal function tests 2. Cardiac
catheterization
Liver function tests 3. Holter monitor
B-type natriuretic peptide

ECG
Chest x-ray
Echocardiogram
CXR
Cardiomegaly
Vascular redistribution
Kerley B lines
Interstitial edema
Peri-bronchial cuffing
Effusions

Chest radiographs in patients with abrupt onset are
usually helpful but can be limited because a delay of as
long as 12 hours is possible from the onset of dyspnea due
to acute heart failure to the development of classic
abnormal findings on radiographs.
Classic radiographic findings demonstrate cardiomegaly

(in patients with underlying CHF) and alveolar edema with
pleural effusions and bilateral infiltrates in a butterfly
pattern. The other signs are loss of sharp definition of
pulmonary vasculature, haziness of hilar shadows, and
thickening of interlobular septa (Kerley B lines).
In long standing biventricular chronic heart failure, chest

radiographs may only show cardiomegaly without alveolar
edema or pleural effusions due to adaptive lung
mechanism with increased arterial vasoconstriction and
lymphatic drainage.
Electrocardiography
o The presence of left atrial enlargement and LV

hypertrophy is sensitive (although nonspecific)
for chronic LV dysfunction.
o ECG may suggest an acute tachyarrhythmia or

bradyarrhythmia.
o ECG may aid in the diagnosis of acute myocardial

ischemia or infarction as the cause of heart
failure or may suggest the likelihood of prior
myocardial infarction or presence of coronary
artery disease as the cause of heart failure.
o ECG is of limited help when an acute valvular

abnormality or LV systolic dysfunction is
considered to be the cause of heart failure;
however, the presence of left bundle branch

block (LBBB) on an ECG is a strong marker for
diminished LV systolic function
Echocardiogram
Chamber
enlargement
Wall motion
abnormalities
Diminished ejection
fraction
Possible LVH
Possible valvular
problems
Assess diastolic dysfunction

Treatment Goals
Improve symptoms
A. Enhance well-being and quality of life
B. Increase exercise tolerance
Improve survival
A. Prevent progressive heart failure
B. Prevent sudden death
C. Prevent thromboembolic episodes
Treatment ::

Oxygen nasal, BiPAP, intubation
Fluid Balance
Restrict fluid- 1000ml daily/ salt intake

Monitor Input/Outputs and daily weight
Dialysis if needed -Critical renal failure patients
Aspirin 75mg
Promoting Rest and Activity
Bed rest or limited activity may be necessary
during the acute phase
Provide an overbed table close to the patient to
allow resting the head and arms
Use pillows for added support.
Gradual ambulation is encouraged to prevent risk
of venous thrombosis and embolism due to
prolonged immobility
Activities should progress through dangling,
sitting up on a chair and then walking in
increased distances under close supervision.
Assess for signs of activity intolerance (dyspnea,
fatigue and increased pulse rate that does not
stabilize readily)
Providing Skin Care
Edematous skin is poorly nourished and
susceptible to pressure sores
Change position at frequent intervals
Assess the sacral area regularly
Use protective devices to prevent pressure sores
Promoting Elimination
Advise to avoid straining at defecation which
involves Valsalva manoeuvre.
Administer laxative as ordered
Encourage use of bedside commode

Preload Reduction
Loop diuretics Lasix 20-200mg IV (q 6-8 hours)
Nitrates -Nitroglycerin IV:10-200 mcg/min
ACEi / ARB Captopril 6.25-50mg PO q8h
Enalapril 2.5-20mg PO BID
Afterload Reduction
IV NTG, Nitroprusside
Hydralazine 10-100mg PO q6-8 h
ACE-I / ARB
Ionotropic Support
Dopamine / Dobutamine 500mg in 250cc D5W
3.10 cg/kg/min

Amrinone / Milrinone n Digoxin (chronic)
Mechanical (ABP) Cardiogenic shock

unresponsive to above tx
A.-----------Diuretics
volume overload , sodium overload ,

preload reduction
Advantages
Highly effective in most classes
Essential with fluid retention
Well tolerated, simple to use
Disadvantages
Electrolyte abnormalities Na, k ,Ca ,Mg
Hypovolemia, hypotension, renal dysfunction
Activation of neurohormaonal system
AIM----Elimination of symptoms and/or signs of

congestion
Avoid volume depletion
A. Postural hypotension B. Increase in heart rate
C. Increase in BUN/Cr D. Neuroendocrine

activation
Thiazide Diuretics-----Hydrochlorothiazide, Chlorthalidone ,

Metolazone
Loop Diuretics----------Furosemide , Torsemide
Potassium Sparing Diuretics---Spironolactone ,

Triamterene , Amiloride

Spironolactone :
Aldosterone inhibition minimize potassium loss, prevent

sodium and water retention, endothelial dysfunction and
myocardial fibrosis.
B-------------ACE Inhibitors
ACE inhibitors should be the initial treatment

for heart failure
Improve hemodynamic status
Attenuate neurohumoral abnormalities
Improve symptoms, left ventricular ejection

fraction .
Reduce incidence of hospitization
Slow progression
Reduce mortality

Neurohormonal Changes
Decreased angiotensin II.
Reduction in arterial resistance (afterload).
Reduction in venous tension (preload).
Inhibition of cardiac and vascular remodeling .
Increased bradykinin
Decreased or no change in aldosterone
Decreased norepinephrine
Reduction in Sudden Death/Potential Mechanisms
Increase in serum/total body potassium
Decreased adrenergic stimulation

Reduced heart size and decrease in ventricular
hypertrophy
Prevention of myocardial ischemia
Prevention of progressive myocardial damage
FDA Approved
Captopril ,Enalapril ,Lisinopril ,Quinapril

,Trandolapril ,Fosinopril
Adverse effects :
Dry irritating persistent cough
Hyperkalemia
Angioedema
Fetal toxicity
C---------------Beta Blockers

Primary mechanism is inhibition of down regulation of
beta receptors
Additional mechanisms
A. Restore receptor density
B.Protect against cardiotoxicity of catecholeamines
C. Improve systolic/diastolic function in ischemic

myocardium
First Generation: Beta 1 and Beta 2
Propranolol/Timolol
Second Generation: Beta 1
Metoprolol/Atenolol
Third Generation: Vasodilating Properties
Carvedilol
Improve symptoms and clinical class
Degree of benefit appears to relate to degree of

disability before treatment
Should be used in all stable Class II/III patients unless

contraindicated
Treatment should not be initiated in patients with

acutely decompensated CHF
Clinical response may take 2 to 3 months
Risks of Treatment
Hypotension Fluid retention and

worsening CHF

Bradycardia and heart block

Start at low dose and monitor for bradycardia
Carvedilol and Metoprolol are the most commonly

used for CCF amongst beta blockers
D------------Angiotensin Receptor AT-1 blockers (ARB) :
Losartan, Irbesartan, Candesartan
Competitive antagonists of Angiotensin II (AT-1).
No inhibition of ACE or Cough.

E--------------Vasodilators :
Isosorbide dinitrate and hydralazine also used

specially in patients who cannot tolerate ACE
inhibitors.
Amlodipine and prazosin are other vasodilators can

be used in CCF.

F-------Cardiac glycosides : Digoxin :
Inhibition of Na/K ATPase pump increase intracellular

sodium concentration eventually increase cytosolic
calcium.
It restores the vagal tone and abolishes the

sympathetic over activity.
Has positive inotropic (strengthens force of cardiac

contractility) and negative chronotropic effects
(decreases heart rate.

Increase the refractoriness of AV node thus decrease
ventricular response to atrial rate.
Digoxin is used as a first-line drug in patients with

congestive heart failure who are in atrial fibrillation.
Adverse effects / Precautions :
Nausea, vomiting, gynecomastia, visual disturbances

and psychosis.
Ventricular bigeminy, AV block and

bradycardia.
Antidote for Toxicity: Digibind

Nursing Responsibilities
Assess heart rate before administration;
if below 60 bpm or above 120 bpm,
withhold the drug.
Monitor serum potassium
Assess for signs of Digitalis toxicity
- Bradycardia
- GI manifestations (anorexia, nausea,
vomiting and diarrhea)
- Dysrrhythmias
- Altered visual perceptions
- In males: gynecomastia, decreased
libido and impotence
Amiodarone and verapamil can increase the plasma
concentration of digoxin by inhibiting its excretion
IN DIASTOLIC FAILURE;
USE B-BLOCKER, ACE-I , CALCIUM CHANNEL BLOCKER

RATE LIMITING
Difficult to treat
Diuretics for volume overload. Avoid volume

depletion
Prevent tachycardia
Rate-limiting calcium channel blockers first choice
Beta 1 beta blockers second choice
ADVERSE PROGNOSTIC MARKERS IN CHRONIC HEART

FAILURE
Old Age,
Severity of heart failure (NYHA class)

Left ventricular dysfunction,
Diabetes Mellitus,
Raised creatinine,
Hyponatremia , Hypoalbuminaemia,Anaemia
Presence of arrhythmia : AF / VT
Causes of Mortality in Heart Failure
Pump failure
Arrhythmia
Severe Anaemia
Associated serious co-morbidities i.e. Renal failure
Cardiac Inotropes =
Dopamine acts at a variety of receptors (dose

dependant)
Rapid elimination- can only be administered as a

continuous infusion
Dobutamine
Stimulates beta-adrenergic receptors and produces a

positive inotropic response
Unlike the vasoconstriction seen with high doses of

dopamine, dobutamine produces a mild vasodilatation
.
PDE Phosphodiesterase inhibitors
Inamrinone (amrinone) and Milrinone (bipyridines)

Acts by inhibiting the enzyme Phosphodiesterase
Thus lead to increase of intracellular concentrations

of cAMP
cAMP is responsible for the conversion of inactive

protein kinase to active form
Protein kinases are responsible for phosphorylation of

Ca channels
Thus causing increased Ca entry into the cell.
MECHANISM OF ACTION:
Increase myocardial contractility by increasing the Ca

influx during AP
Also have vasodilating effect
Selective for PDE isoenzyme-3 (found in cardiac and

smooth muscle)
ADVERSE RECTIONS
Inamrinone: nausea, vomiting, arrhythmias,

thrombocytopenia and liver enzyme changes
Withdrawn in some countries
Milrinone: arrhythmias, less likely to cause other ADR
Niseritide
Brain (B-type) natriuretic peptide (BNP) is secreted

constitutively by ventricular myocytes in response to
stretch
BNP binds to receptors in the vasculature, kidney, and

other organs, producing potent vasodilation with

rapid onset and offset of action by increasing levels of
cGMP
Niseritide is recombinant human BNP approved for

treatment of acute decompensated CHF.
It reduces systemic and pulmonary vascular

resistances, causing an indirect increase in cardiac
output and diuresis.
Effective in HF because cause reduction in preload

and afterload
ADR- hypotension
OTHERS;
Implantable cardioverter-defibrillator
Pacemakers, Biventricular pacemaker
Heart transplant
Cardiac Resynchronisation Therapy


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Heart Failure

MAGDI AWAD SASI 2013

1 MAGDI AWAD SASI HEART FAILURE 2013

HF is a clinical syndrome including circulatory

An inadequate or decreased cardiac output which

Frequency : United States

Blacks are 1.5 times more likely to die of CHF than

Prevalence is greater in males than in females in

3 MAGDI AWAD SASI HEART FAILURE 2013

Prevalence of CHF increases with increasing age and

Approximately 30-40% of patients with congestive

50% of HF patients will die 5 years after the

The most common cause of death is progressive heart

Patients with coexisting insulin-dependent diabetes

4 MAGDI AWAD SASI HEART FAILURE 2013

5 MAGDI AWAD SASI HEART FAILURE 2013

6 MAGDI AWAD SASI HEART FAILURE 2013

Rt. Vs Lt. sided HF

Low Vs High output HF

7 MAGDI AWAD SASI HEART FAILURE 2013

stenosis/regurgitation( RHD, infective endocarditis)

5. Rhythm- atrial fibrillation

The patient present with chest symptoms which may delay

Failure of forward flow from left ventricle into the aorta

9 MAGDI AWAD SASI HEART FAILURE 2013

LVF can be acute or chronic depending on the underlying

LVF= CHEST SYMTOMS= D/D OF ALL LUNG DISEASES=

LVF symptoms are:

Dyspnea upon exertion: This has been found to be the

Orthopnea and paroxysmal nocturnal dyspnea (PND):

Cough: Cough that produces pink, frothy sputum is

Wheezing= new onset of wheezing above age of 60

Chest pain or tightness especially if the cause is

Non specific symptoms of low COP

10 MAGDI AWAD SASI HEART FAILURE 2013

11 MAGDI AWAD SASI HEART FAILURE 2013

The patient present with abdominal symptoms which may

Failure of forward flow from right ventricle into the

Failure of the right ventricle to maintain a normal output

Since the right ventricle does not empty completely, it

12 MAGDI AWAD SASI HEART FAILURE 2013

RVF can be acute or chronic depending on the underlying

RVF= ABDOMENAL SYMTOMS= D/DOF ABDOMENAL

Right-sided or right ventricular (RV) heart failure usually

RVF symptoms are:

These symptoms are caused by internal abdominal

And can be mistaken for local abdominal pathology.

RVF is caused by:

13 MAGDI AWAD SASI HEART FAILURE 2013

2. Pulmonary hypertension caused by chronic lung

Patients with mild heart failure appear to be in

Patients with recent onset of heart failure are

Chronic marked elevation of systemic venous

14 MAGDI AWAD SASI HEART FAILURE 2013

In mild or moderate heart failure, stroke volume

With very severe heart failure, particularly if

Evidence of increased adrenergic activity

Increased adrenergic activity is manifested by

Diastolic arterial pressure may be slightly

Pulmonary rales =LVF

Rales heard over the lung bases( bilateral basal

The absence of rales certainly does not exclude

15 MAGDI AWAD SASI HEART FAILURE 2013