CLINICAL ASPECT OF HEART

FAILURE; PULMONARY EDEMA, HIGH-

OUTPUT FAILURE

dr. Novita, Sp. JP., FIHA

SMF Cardiologi RSUD dr. Zainoel Abidin Pemerintah Aceh

Fakultas Kedokteran Universitas Syiah Kuala, Banda Aceh
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. Tachyarrhythmias, most commonly AF. Reduce
the time available for ventricular filling or
ventricular compliance
2. 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. Reduce symptoms
2. Prolong survival
3. 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. Septal, producing Kerley lines
2. Perivascular, producing loss of sharpness of the
central and peripheral vessels
3. 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. 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
2. 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-α 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. Increased capillary pulmonary pressure
2. Hypoalbuminemia
3. Increased negative interstitial pressure
4. 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. Impairment of left atrial outflow
2. LV systolic or diastolic dysfunction
3. LV volume overload
4. LV outflow obstraction
 Diagnosis
1. Suffocation and oppression in the chest intensifies
2. Elevates HR and BP
3. 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
doesn’t 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