CLINICAL ASPECT OF HEART FAILURE;

PULMONARY EDEMA, HIGH-OUTPUT

FAILURE

dr. Faisal, Sp.PD

DEFINITION

Heart failure is a complex clinical syndrome

that result from any structural or functional
cardiac disorder that impair the ability of the
ventricle to fill with or eject blood.

Prevalence and incidence

1 to 2 % of persons 45 to 54 years
10 % of individual older than 75 years

Framingham Criteria for Heart Failure

Major criteria

Paroxysmal nocturnal dyspnea

Neck vein distention

Rales

Radiographic cardiomegaly

Acute pulmonary edema

S3 gallop

Increased central venous pressure > 16 cm H2O

Circulation time > 25 sec

Hepatojugular reflux

Pulmonary edema, visceral congestion, or cardiomegaly at autopsy

Weight loss > 4.5 kg in 5 day in response to treatment of heart failure

Minor criteria
Bilateral ankle edema
Nocturnal cough
Dyspnea on ordinary exertion
Hepatomegaly
Pleural effusion
Decrease in vital capacity by one third from maximal
value recorded
Tachycardia (rate > 120 beats/min)

Form and causes of HF

Backward failure hypothesis

The ventricle fails to discharge its contents,
blood accumulates and pressure rises in the
atrium and venous system emptying into it

Following sequence :

Ventricle end diastolic volume and pressure increase

Volume and pressure rise in the atrium
The atrium contracts more vigorously
The pressure in the venous and capillary beds rises
Transudation of fluid from the capillary bed into the
interstitial space (pulmonary or systemic) increase

Forward failure hypothesis, relates clinical

manifestations of HF to inadequate delivery
of blood into the arterial system
Result in diminished perfusion of vital organs,
including brain and kidney

Right side versus left side HF

Symptom secondary to pulmonary congestion

initially predominate in patients with left
ventricular infarction, hipertension,aortic or
mitral valve disease manifest left side HF
Fluid accumulation, ankle edema,congestive
hepatomegaly and pleural effusion occur
exhibit right side HF

Fluid retention

Due to reduction in glomerular filtration rate,

activation of neurohormonal system, RAAS
and sympatetic nervous system
Combination of impaired hepatic
function,further raising plasma concentration
and augmenting the retention of sodium and
water

Acute versus chronic HF

The clinical manifestation of HF depend

importantly on the rate
The syndrome develops and specifically
on whether sufficient time has elapsed
for compensatory mechanism to become
operative and for fluid to accumulate in
the interstitial space

Low output vs High output HF

Low output HF : systemic vasoconstriction

with cold, pale, cyanotic extremities.
Marked reduction in the stroke volume,
reflected by narrowing pulse pressure
Congenital, valvular, rheumatic, hypertensive,
coronary and cardiomyopathy

High output HF, the extremities are usually

warm, flushed and the pulse pressure is
widened or at least normal
High cardiac output state : thyrotoxicosis,
arteriovenous fistulas,beri-beri, paget disease
of bone, and anemia

Systolic vs diastolic HF

Systolic HF : abnormality in systolic function

leading to a defect in the expulsion of blood
Result from inadequate cardiac output or salt
and water retention

Diastolic HF : abnormality in the diastolic

function, which ability of the ventricle to
accept blood is impaired
Due to slowed or incomplete ventricular
relaxation transient in acute ischemia or
sustained as in myocardial hypertrophy or
restrictiv cardiomyopathy

Underlying causes of HF

Structural abnormality, congenital or acquired

that affect the peripheral and coronary
vessels, pericardium, myocardium or cardiac
valves
Increased hemodynamic burden and
myocardial stress or coronary insufficiency
responsible for HF

Precipitating causes of HF (1)

Inappropriate reduction of therapy

Dietary excess of sodium frequent causes of
cardiac decompensation
Self discontinuation or physician withdrawal of
effective pharmacotherapy such as ACE-I, diuretic
or digoxin can precipitate HF

Precipitating causes of HF (2)

Arrhythmias, may precipitate HF through

several mechanism :
1.

2.

Tachyarrhythmias, most commonly AF. Reduce

the time available for ventricular filling or
ventricular compliance
Marked bradikardia, in patient with underlying
heart disease

Precipitating causes of HF (3)

3. Dissociation between atrial and ventricular
contraction, in patients with impaired ventricular
filling related to cardiac hypertrophy e.g systemic
hypertension, aortic stenosis and hypertrophic
cardiomyopathy
4. Abnormal intraventricular conduction, such as
ventricular tachycardia

Precipitating causes of HF (4)

Myocardial ischemia or infarction

Systemic infection
Pulmonary embolism
Physical, emotional and environtmental stress
Cardiac infection and inflammation
Development of an unrelated illness, e.g acute
on chronic renal failure

Precipitating causes of HF (5)

Administration of myocardial depressant or

salt retaining drugs. Such as verapamil,
diltiazem many anti arrythmic agents,
inhalation and intravenous anesthetics and
antineoplastic drugs, estrogen, NSAID

Precipitating causes of HF (6)

Cardiac toxin
Alcohol is a potent myocardial depressant and
may be responsible for development
cardiomyopathy
High output states
Patient with underlying heart disease such as
valvular heart disease or hyperkinetic
circulatory stress such as pregnancy or anemia

Clinical manifestation

Symptom
Respiratory distress
1. Exertional dyspnea
2. Orthopnea
3. Paroxysmal nocturnal dyspnea
4. Dyspnea at rest
5. Acute pulmonary edema

Mechanism of exercise intolerance

Abnormalities in central and peripheral

cardiovascular function
Development of dyspnea related to pulmonary
vascular congestion
Failure of the cardiovascular system to
provide sufficient blood flow to exercising
muscles

Other symptom

Fatique and weakness

Urinary symptom
Nocturia, When the patient rest in the position
recumbent at night renal vasoconstriction
diminishes and urine formation increase
Oliguria, suppression of urine formation as a
consequence of severely reduced cardiac output

Other symptom

Cerebral symptom
Symptom of predominant right sided heart
failure
Congestive hepatomegaly
Other gastrointestinal symptoms

Quality of life
The three main goals of treatment for heart
failure :
1.
2.
3.

Reduce symptoms
Prolong survival
Improve quality of life

A good quality of life implies the ability to live

as one wants, free of physical, social,
emotional and economic limitations

Physical findings

General appearance
1.Dyspneic during and immediately after moderate activity
2.Uncomfortable if lie flat without elevation of the head
3.Anxious
4.Marked elevation of systemic venous pressure
5.Cyanosis,icterus, a malar flush,and abdominal distention
6. The pulse may be rapid, weak and thready

Physical findings

Increased adrenergic activity : pallor,

coldness,cyanosis,diaphoresis,sinus
tachycardia
Pulmonary rales, result from transudation of
fluid into the alveoli and then into the airways
Systemic venous hypertension, by inspection
of jugular veins

Physical findings

Hepatojugular reflux
Congestive hepatomegaly
Edema, symmetrical and pitting and generally occurs
first in the dependent portions of the body
Hydrothorax (pleural effusion) : occur as increased
amounts of fluid in the lung interstitial spaces exit
across the visceral pleura
Ascites

Cardiac findings

Cardiomegaly
Gallop sounds : Protodiastolic sounds,
occuring 0,13 to 0,16 second after S2
Pulsus alternans : regular rhythm with
alternating strong and weak ventricular
contractions
Accentuation of P2 and systolic murmur

Abnormal response to the valsava maneuver

Fever
Cardiac cachexia
Cheyne-Stokes respiration (periodic or cyclic
respiration) : combination of the depression in
the sensitivity of the respiratory center to
CO2 and left ventricular failure

Pathological findings

Lungs : enlarged, firm and dark and may be

filled with bloody fluid. Pulmonal vessels
show medial hypertrophy and intimal
hyperplasia
Liver, cardiac cirrhosis (cardiac sclerosis) is a
result of sustained, chronic severe HF.

Laboratory findings

Serum electrolytes
1.Dilutional hyponatremia, caused by prolonged sodium
restriction
2. Serum potassium are usually normal, hypokalemia caused
by prolonged administration of kaliuretic diuretics
3. Secondary hyperaldosteronism may also contribute
hypokalemia
4. Hyperkalemia, if severe HF show marked reduction in
GFR
5. Hypophosphatemia
6. Hypomagnesemia

Laboratory findings

Renal function
Proteinuria
High urine specific gravity
BUN and creatine levels moderately elevated

Liver function test

Abnormal values of AST, ALT, LDH and other liver
enzymes
Hyperbilirubinemia, both, direct and indirect
Hypoalbuminemia

Laboratory findings

Hematological studies
Anemia, due to increase plasma volume
(hemodilution) or decreased cell mass (true
anemia)
Leukocytosis occur following acute MI. In acute HF
or hemodynamic instability, leukocytosis may
suggest the presence of infective endocarditis or
pulmonary embolism

Chest radiography

Normal pulmonary and venous pressure, the

lung bases are better perfused than the apices
in the erect position
Interstitial pulmonary edema occurs, when
pulmonary capillary pressure exceed 20 to 25
mmHg

Chest radiography

Several varieties of edema :

1.
2.
3.

Septal, producing Kerley lines

Perivascular, producing loss of sharpness of the
central and peripheral vessels
Subpleural, producing spindle shaped
accumulation of fluid between the lung and
adjacent pleural surface

If exceeds 25 mmHg, alveolar edema

(butterfly pattern)

Prognosis

Factors have been found to correlate with

mortality in HF :
1.

2.

Clinical, presence of CAD as the etiology of HF,

S3, elevated JVP, low pulse and systolic arterial
pressures,a high NYHA class and reduced
exercise capacity ------- increase mortality
Structural, associated with increased risk of
arrythmias or death

Factors
3.Hemodynamic : Combination of hemodynamic
abnormalities, such as depression of stroke work
associated with elevation filling pressure and
systemic vascular resistance, are associated with
poor pognosis
4.Biochemical : Strong inverse correlation between
survival and plasma level of epinefrin,
angiotensin II, renin, arginin , vasopresin,
ANP,BNP and endothelin-I

Factors
5. Other marker prognosis : Plasma levels of
proinflammatory cytokines,TNF- and IL-6 and
their cognate receptors are elevated in relation to
disease severity and predict averse outcomes

Pulmonary Edema

Mechanism of pulmonary edema

1.

Alveolar capillary membrane

Pulmonary edema : movement of liquid from the blood to
the interstitial space,and in some instances to the alveoli
Alveolar capillary membrane consist :
a. Cytoplasmic projection of capillary
endothelial
cells
b. The interstitial space
c. The lining of the alveolar space

Pulmonary edema
2. Lymphatics

More negative pressure in the peribronchial and

perivascular interstitial space
Increased compliance of non alveolar interstitium
Pumping capacity of the lymphatic channels is
excedeed
Interstitial edema

Sequence of fluid accumulation during

pulmonary edema

Stage 1 : Increase in mass transfer of liquid

and colloid from blood capillaries through the
interstitium
Stage 2 : the filtered load from the pulmonary
capillary is large that the pumping capacity
exceeded
Stage 3 : Distention of the less compliant
interstitial space of the alveolar capillary
septum and resulting in alveolar flooding

Classification of pulmonary edema

Imbalance o starling forces

1.
2.
3.
4.

Increased capillary pulmonary pressure

Hypoalbuminemia
Increased negative interstitial pressure
Primary alveolar capillary barrier damage

Cardiogenic pulmonary edema

PATHOPHYSIOLOGY
Transudation of protein poor fluid into the
lungs secondary to an increase in left atrial
and pulmonary capillary pressure
Stage 1 : distention and recruitment of small
pulmonary vessels secondary to elevation of
left atrial pressure

Stage 2 : Interstitial edema

Stage 3 : Edema, gas exchange is quite
abnormal, with severe hypoxia and often
hypocapnia

Etiology and diagnosis

Etiology
1.
2.
3.
4.

Impairment of left atrial outflow

LV systolic or diastolic dysfunction
LV volume overload
LV outflow obstraction

Diagnosis
1.
2.
3.

Suffocation and oppression in the chest intensifies

Elevates HR and BP
Restricts ventricular filling

Clinical manifestations

Extreme breathlessness suddenly

Anxious,coughs,expectorates pink,frothy
liquid
Sits bolt upright
The respiratory rate is elevated
Alae nasi are dilated
Inspiratory retraction of the ICS and
supraclavicular fossae

Clinical

Often grasp the sides of the bed to allow use

of the accessory muscles of respiration
Loud inspiratory and expiratory gurging
sound
Sweating profuse, skin usually cold,ashen and
cyanotic
On auscultation :ronchi,wheezes and moist
and fine crepitant rales

Differentiation from asthma

There is usually a history of previous similar

episodes
The patients is aware of the diagnosis
Asthmatic patients does not sweat profusely and
arterial hypoxemia
The chest hiperexpanded and hyperresonant
Wheezes are higher pitched and more musical than
in pulmonary edema
Other adventitious sounds such as ronchi and rales
less prominent

Prognosis

The long term prognosis after an episode of

acute pulmonary edema depends on the
underlying cause of pulmonary edema (e.g,
acute MI) and the presence of comorbidities
such as diabetes or end stage renal disease

Pulmonary edema of unknown or

incompletely defined pathogenesis

High altitude pulmonary edema (HAPE)

Neurogenic pulmonary edema
Narcotic overdose pulmonary edema
Pulmonary embolism
Eclampsia
After cardioversion
After anesthesia
After cardiopulmonary bypass
Transfusion related acute lung injury
Hantavirus pulmonary syndrome
Other viral infections

Differential Diagnosis of pulmonary

edema

Cardiogenic (Hemodynamic)
Non cardiogenic ( caused by alterations in the
alveolar capillary barrier)

HIGH OUTPUT FAILURE

Anemia
Chronic anemia : is associated with high
cardiac output when Hb is less than 8 gm/dl
Anemic patient oftes has pale,paleness
conjunctiva,mucous membranes and palmar
creases are helpful

Anemia
Arterial pulse are bounding
Pistol shot sounds can be heard over the
femoral arteries
Sub ungual capillary pulsations
Medium pitched mid systolic murmur
Heart sounds are accentuated

Management

Treatment HF associated severe anemia

should be specific for the anemia
Diuretics and cardiac glycosides, when HF is
present

Systemic arteriovenous fistulas

Congenital or acquired (post traumatic or

iatrogenic)
The physical findings depend on the
underlying disease, location,size of the shunt
In general : widened pulse pressure, brisk
carotid and peripheral arterial pulsations and
mild tachycardia

Systemic AV fistulas

The extremities are warm and flushed

The branham sign (Nicoladoni-Branham
sign), consist of slowing of the HR after
manual compression of the fistula
The decrease in HR after fistula occlusion
correlates with the flow in the fistula

Acquired AV fistulas

These occur most frequently after such

injuries as gunshot wounds and stab wounds
may involve any part of the body
Most frequently the thigh

Congenital AV fistulas

Result from arrest of the normal embryogenic

development of the vascular system and are
structurally similar to embryonic capillary networks
Disfigurement as well as swelling and pain in the
limb
Often present erythema and cyanosis
Angiography to confirming the diagnosis and
determining physical extent of the anomaly

Hyperthyroidism

Increases circulating levels of thyroid

hormone exert direct effects on the
cardiovascular system, HR and contractility
Physical findings : widened pulse pressure,
brisk carotid, peripheral arterial pulsations,
hyperkinetic cardiac apex, and loud first heart
sounds

The hyperkinetic state of hyperthyroidism

doesnt usually lead to HF in the absence of
underlying cardiovascular disease
The high output cardiac failure of
hyperthyroidism is frequently accompanied
by an exacerbated by AF and a rapid ventricle
rate

Beri-beri heart disease

Due to severe thiamine deficiency persisting

for at least 3 month
Deficiency leads to impaired oxidative
metabolism through inhibition of the citric
acid cycle and the hexose monophosphate
shunt and result in lactic acidosis

Beri-beri

Physical findings of the high output state and

usually of severe generalized malnutrition and
vitamin deficiency
Treatment : thiamine up to 100 mg IV
followed by 25 mg/d

Other causes of high output cardiac

failure

Paget disease
Fibrous displasia
Multiple myeloma
Other condition : Pregnancy, renal disease
(glomerulnefritis), cor pulmonale,
acromegaly, polycythemia vera