clinical aspect of heart failure

8/10/2019 Clinical Aspect of Heart Failure

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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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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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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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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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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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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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clinical aspect of heart failure

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