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CLINICAL ASPECT OF HEART
FAILURE; PULMONARY EDEMA, HIGH-
OUTPUT FAILURE
dr. Faisal, Sp.PD
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Prevalence and incidence 1 to 2 % of persons 45 to 54 years
10 % of individual older than 75 years
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Framingham Criteria for Heart FailureMajor 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
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Formand causes of HF
Backward failure hypothesis
The ventricle fails to discharge its contents,
blood accumulates and pressure rises in theatrium and venous system emptying into it
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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
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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
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Right side versus left side HF Symptom secondary to pulmonary congestion
initially predominate in patients with leftventricular infarction, hipertension,aortic ormitral valve disease manifest left side HF
Fluid accumulation, ankle edema,congestivehepatomegaly and pleural effusion occur
exhibit right side HF
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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 andwater
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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
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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
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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
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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 saltand water retention
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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 orrestrictiv cardiomyopathy
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Underlying causes of HF
Structural abnormality, congenital or acquired
that affect the peripheral and coronary
vessels, pericardium, myocardium or cardiacvalves
Increased hemodynamic burden and
myocardial stress or coronary insufficiencyresponsible for HF
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Precipitating causes of HF (1)
Inappropriate reduction of therapy
Dietary excess of sodium frequentcauses of cardiac
decompensation
Self discontinuation or physician withdrawal of
effective pharmacotherapy such as ACE-I, diuretic
or digoxin can precipitate HF
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Precipitating causes of HF (2)
Arrhythmias, may precipitate HF through
several mechanism :
1. Tachyarrhythmias, most commonly AF. Reducethe time available for ventricular filling or
ventricular compliance
2. Marked bradikardia, in patient with underlying
heart disease
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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
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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
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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
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Precipitating causes of HF (6)
Cardiac toxin
Alcohol is a potent myocardial depressant and
may be responsible for developmentcardiomyopathy
High output states
Patient with underlying heart disease such asvalvular heart disease or hyperkinetic
circulatory stress such as pregnancy or anemia
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Clinical manifestation Symptom
Respiratory distress
1. Exertional dyspnea2. Orthopnea
3. Paroxysmal nocturnal dyspnea
4. Dyspnea at rest5. Acute pulmonary edema
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Mechanism of exercise intolerance
Abnormalities in central and peripheral
cardiovascular function
Development of dyspnea related to pulmonaryvascular congestion
Failure of the cardiovascular system to
provide sufficient blood flow to exercisingmuscles
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Other symptom
Fatique and weakness
Urinary symptom
Nocturia, When the patient rest in the positionrecumbent at night renal vasoconstriction
diminishes and urine formation increase
Oliguria, suppression of urine formation as a
consequence of severely reduced cardiac output
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Other symptom
Cerebral symptom
Symptom of predominant right sided heart
failureCongestive hepatomegaly
Other gastrointestinal symptoms
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Quality of life
The three main goals of treatment for heart
failure :
1. Reduce symptoms2. Prolong survival
3. Improve quality of life
A good quality of life implies the ability tolive as one wants, free of physical, social,
emotional and economic limitations
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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
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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 inspectionof jugular veins
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Physical findings
Hepatojugular reflux
Congestive hepatomegaly
Edema, symmetrical and pitting and generally occursfirst 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
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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
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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 CO2and left ventricular failure
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Pathological findings
Lungs : enlarged, firm and dark and may be
filled with bloody fluid. Pulmonal vessels
show medial hypertrophy and intimalhyperplasia
Liver, cardiac cirrhosis (cardiac sclerosis) is a
result of sustained, chronic severe HF.
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Laboratory findings Serum electrolytes
1.Dilutional hyponatremia, caused by prolonged sodiumrestriction
2. Serum potassium are usually normal, hypokalemia causedby prolonged administration of kaliuretic diuretics
3. Secondary hyperaldosteronism may also contributehypokalemia
4. Hyperkalemia, if severe HF show marked reduction inGFR
5. Hypophosphatemia
6. Hypomagnesemia
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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
enzymesHyperbilirubinemia, both, direct and indirect
Hypoalbuminemia
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Laboratory findings
Hematological studies
Anemia, due to increase plasma volume
(hemodilution) or decreased cell mass (trueanemia)
Leukocytosis occur following acute MI. In acute HF
or hemodynamic instability, leukocytosis may
suggest the presence of infective endocarditis orpulmonary embolism
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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
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Chest radiography
Several varieties of edema :
1. Septal, producing Kerley lines
2. Perivascular, producing loss of sharpness of thecentral and peripheral vessels
3. Subpleural, producing spindle shapedaccumulation of fluid between the lung andadjacent pleural surface
If exceeds 25 mmHg, alveolar edema(butterfly pattern)
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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 ofarrythmias or death
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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
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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
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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
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Sequence of fluid accumulation during
pulmonary edema
Stage 1 : Increase in mass transfer of liquidand colloid from blood capillaries through theinterstitium
Stage 2 : the filtered load from the pulmonarycapillary is large that the pumping capacityexceeded
Stage 3 : Distention of the less compliantinterstitial space of the alveolar capillaryseptum and resulting in alveolar flooding
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Classification of pulmonary edema
Imbalance o starling forces
1. Increased capillary pulmonary pressure
2. Hypoalbuminemia3. Increased negative interstitial pressure
4. Primary alveolar capillary barrier damage
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Cardiogenic pulmonary edema
PATHOPHYSIOLOGY
Transudation of protein poor fluid into the
lungs secondary to an increase in left atrialand pulmonary capillary pressure
Stage 1 : distention and recruitment of small
pulmonary vessels secondary to elevation ofleft atrial pressure
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Stage 2 : Interstitial edema
Stage 3 : Edema, gas exchange is quite
abnormal, with severe hypoxia and oftenhypocapnia
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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 intensifies2. Elevates HR and BP
3. Restricts ventricular filling
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Clinical manifestations
Extreme breathlessness suddenly
Anxious,coughs,expectorates pink,frothyliquid
Sits bolt upright
The respiratory rate is elevated
Alae nasi are dilated
Inspiratory retraction of the ICS andsupraclavicular fossae
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Clinical
Often grasp the sides of the bed to allow use
of the accessory muscles of respiration
Loud inspiratory and expiratory gurgingsound
Sweating profuse, skin usually cold,ashen and
cyanotic On auscultation :ronchi,wheezes and moist
and fine crepitant rales
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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 andarterial 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
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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
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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
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Differential Diagnosis of pulmonary
edema
Cardiogenic (Hemodynamic)
Non cardiogenic ( caused by alterations in the
alveolar capillary barrier)
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HIGH OUTPUT FAILURE
Anemia
Chronic anemia : is associated with high
cardiac output when Hb is less than 8 gm/dlAnemic patient oftes has pale,paleness
conjunctiva,mucous membranes and palmar
creases are helpful
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Anemia
Arterial pulse are bounding
Pistol shot sounds can be heard over the
femoral arteriesSub ungual capillary pulsations
Medium pitched mid systolic murmur
Heart sounds are accentuated
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Management
Treatment HF associated severe anemia
should be specific for the anemia
Diuretics and cardiac glycosides, when HF ispresent
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Systemic arteriovenous fistulas
Congenital or acquired (post traumatic or
iatrogenic)
The physical findings depend on theunderlying disease, location,size of the shunt
In general : widened pulse pressure, brisk
carotid and peripheral arterial pulsations andmild tachycardia
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Systemic AV fistulas
The extremities are warm and flushed
The branham sign (Nicoladoni-Branham
sign), consist of slowing of the HR aftermanual compression of the fistula
The decrease in HR after fistula occlusion
correlates with the flow in the fistula
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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
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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 anddetermining physical extent of the anomaly
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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
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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
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Beri-beri heart disease
Due to severe thiamine deficiency persisting
for at least 3 month
Deficiency leads to impaired oxidativemetabolism through inhibition of the citric
acid cycle and the hexose monophosphate
shunt and result in lactic acidosis
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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
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Other causes of high output cardiac
failure
Paget disease
Fibrous displasia
Multiple myeloma Other condition : Pregnancy, renal disease
(glomerulnefritis), cor pulmonale,
acromegaly, polycythemia vera
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