Transcript Heart Failure Cor Pulmonale

Heart Failure
Cor Pulmonale
Eugenio Jose F. Ramos, MD, FPCP, FPCC
The Medical City
Coronary
Thrombosis
NSTEMI, AMI
CAD
Myocardial Ischemia
Atheroscleorsis
LVH
Risk Factors
Diabetes
Hypertension
Smoking
Death
Arrhythmia
Muscle Loss
Remodelling
LV Dilatation
Heart Failure
Progressive
Death
Responses to hemodynamic overload
Pressure overload
Systolic wall stress
Volume overload
Diastolic wall stress
Mechanical transducers
Extra- & intracellular signals
Ventricular remodeling
Parallel sarcomeres
Series sarcomeres
Concentric LVH
Eccentric LVH
Chain of Events after M.I. leading to
Cardiovascular Mortality
Myocardial Infarction
Arrhythmia
Loss of Muscle
Remodeling
Neurohormonal
Activation
Sudden Death
Ventricular
Dilatation
Heart Failure
Death
Heart Failure
Definition

inherited or acquired abnormality of
cardiac structure and/or function
leading to a constellation of clinical
symptoms (dyspnea and fatigue) and
signs (edema and rales) that lead to
frequent hospitalizations, a poor
quality of life, and a shortened life
expectancy.
Epidemiology

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
overall prevalence of HF in the adult
population in developed countries is 2%.
prevalence follows an exponential pattern,
rising with age, and affects 6–10% of people
over the age of 65.
relative incidence of HF is lower in women
than in men but women constitute at least
half of the cases of HF because of their
longer life expectancy.
Category of Heart Failure
(1)
(2)
HF with a depressed ejection fraction
(EF) -commonly referred to as
systolic failure
HF with a preserved EF - commonly
referred to as diastolic failure.
Etiology


coronary artery disease (CAD) has
become the predominant cause in men
and women and is responsible for 60–
75% of cases of HF.
Hypertension contributes to the
development of HF in 75% of patients,
including most patients with CAD
Progression from hypertension to
congestive heart failure
Obesity
LVH
Diabetes
Diastolic
Dysfunction
CHF
Hypertension
MI
Smoking
Death
Systolic
Dysfunction
Dyslipidemia
Diabetes
Left Ventricular
Subclinical
Overt Heart
Remodeling
Left Ventricular
Failure
Dysfunction
Time, Decades
Time, mo
Global Considerations
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Rheumatic heart disease remains a major cause of
HF in Africa and Asia, especially in the young.
Hypertension is an important cause of HF in the
African and African-American populations.
Chagas' disease is still a major cause of HF in
South America.
CAD emerging as the single most common cause of
HF in Western Europe and North America
Prognosis

difficult to predict prognosis in an
individual
– functional status is an important predictor
of patient outcome
patients with symptoms at rest (NYHA) class
IV have a 30–70% annual mortality rate
 patients with symptoms with moderate
activity (NYHA class II) have an annual
mortality rate of 5–10%

Pathogenesis
HF is a progressive disorder that is
initiated after an index event causing
– damage the heart muscle, with a
resultant loss of functioning cardiac
myocytes
– alternatively disrupts the ability of the
myocardium to generate force preventing
the heart from contracting normally

index event
– may have an abrupt onset (as in the case
of an acute myocardial infarction)
– it may have a gradual or insidious onset
(as in the case of hemodynamic pressure
or volume overloading)
– it may be hereditary, as in the case of
many of the genetic cardiomyopathies.
Pathogenesis of HF
– begins after an index event produces an
initial decline in the heart's pumping
capacity.
– Following initial decline in pumping
capacity, a variety of compensatory
mechanisms are activated, including the
adrenergic nervous system, the reninangiotensin-aldosterone system and the
cytokine system.
Compensatory
mechanisms in HF
– short term:

to restore cardiovascular function to a normal
homeostatic range →asymptomatic pt.
– long term:

sustained activation of these systems →
secondary end-organ damage within the
ventricle→ worsening left-ventricular
remodeling → subsequent cardiac
decompensation.
Activation of
Neurohormonal
Mechanisms in
Heart Failure
Activation of Neurohormonal Systems
decreased cardiac output results in an "unloading" of high-pressure
baroceptors in the left ventricle, carotid sinus, and aortic arch
activation of afferent signals to the CNS
stimulate the release of AVP from the
posterior pituitary (potent
vasoconstrictor increasing permeability
of renal collecting ducts)
activate efferent sympathetic
nervous system pathways (heart,
kidney, peripheral vasculature,
skeletal muscles.
Activation of renin-angiotensinaldosterone system
reabsorption of free water
salt & water retention, vasoconstriction, myocyte
hypertrophy, cell death, and myocardial fibrosis.
Neurohormonal Activation
Following Myocardial Damage
Myocardial Damage
Renin
Stimulation
Plasma
Angiotensin II
Aldosterone
Sodium
Retention
Sympathetic
Stimulation
Neural Norepinephrine
Release
Vasoconstriction
Preload
Afterload
Vascular
Congestion
Myocardial
Function
Vasopressin
Stimulation
Plasma
Vasopressin
Water
Retention
Ventricular remodeling


refers to the changes in LV mass, volume,
shape, and composition of the heart that
occur following cardiac injury and/or
abnormal hemodynamic loading conditions.
may contribute independently to the
progression of HF by virtue of the
mechanical burdens that are engendered by
the changes in the geometry of the
remodeled LV
LV Remodeling Following Myocardial Infarction
Dynamics of LV Remodeling
MYOCARDIAL INFARCTION
Neurohormonal
Activation
Systolic Ejection
LVEDV
LVEDP
X
X
Cardiac Output
WALL SRESS
Non-infarcted Segment:
Regional Hypertrophy
Infarcted Segment:
Infarct Expansion
HEART FAILURE
Death
PROGRESSION TO HEART
FAILURE & DEATH
Diseased Myocardium + Neurohormonal Activation
Pathophysiology of myocardial remodeling: Transition
from compensated hypertrophy to HF
Causes of LV Remodelling
(1)
Myocyte hypertrophy
concentric hypertrophy – pressure overload (AS,
HPN)
eccentric hypertrophy – volume overload (AR, MR)
(2) Alterations in the contractile properties of the
myocyte
Progressive loss of contractile function leads to failing heart
(3) Progressive loss of myocytes through necrosis,
apoptosis, and autophagic cell death
(4) adrenergic desensitization
Marked reduction in beta adrenergic receptor density which
may cause increased levels of NE causing sustained
adrenergic stimulation to an energy starved myocardium
(5) abnormal myocardial energetics and
metabolism
(6) reorganization of the extracellular matrix with
dissolution of the organized structural
collagen weave surrounding myocytes and
subsequent replacement by an interstitial
collagen matrix that does not provide
structural support to the myocytes
Systolic Dysfunction
– Impaired ability of the myocyte to
contract contributing to depressed LV
systolic function
- due to sustained neurohormonal
activation resulting in transcriptional and
posttranscriptional changes in the genes
and proteins that regulate excitationcontraction coupling and cross-bridge
interaction
Diastolic Dysfunction

Impaired myocardial relaxation
– reductions in ATP concentration, as
occurs in ischemia may lead to slowed
myocardial relaxation.

LV filling is delayed because LV compliance is
reduced (e.g., from hypertrophy or fibrosis),
LV filling pressures will similarly remain
elevated at end diastole
– increase in heart rate disproportionately
shortens the time for diastolic filling,
which may lead to elevated LV filling
pressures particularly in noncompliant
ventricles

Elevated LV end-diastolic filling pressures
result in increases in pulmonary capillary
pressures
– can occur alone or in combination with
systolic dysfunction in patients with HF
Clinical Manifestations
Cardinal symptoms
1. Fatigue
•
•
low cardiac output
skeletal-muscle abnormalities and other
noncardiac comorbidities (e.g., anemia)
may also contribute to this symptom
2. Dyspnea
 occurs on exertion in early stages
 occurs with less strenuous activity but may
occur even at rest with disease progression
 multi-factorial cause
– reductions in pulmonary compliance, increased
airway resistance, respiratory muscle and/or
diaphragm fatigue, and anemia.
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important mechanism is pulmonary
congestion with accumulation of interstitial
or intra-alveolar fluid, which activates
juxtacapillary J receptors, stimulating rapid,
shallow breathing
may become less frequent with the onset of
right ventricular (RV) failure and tricuspid
regurgitation.
Other Symptoms
Orthopnea
 dyspnea occurring in the recumbent position
 usually a later manifestation of HF than is
exertional dyspnea.
 It results from the redistribution of fluid
from the splanchnic circulation and lower
extremities into the central circulation
during recumbency, with a resultant
increase in pulmonary capillary pressure.
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Nocturnal cough is a frequent
manifestation of this process
generally relieved by sitting upright or
by sleeping with additional pillows.
is a relatively specific symptom of HF
but it may occur in patients with
abdominal obesity or ascites and in
patients with pulmonary disease
whose lung mechanics favor an
upright posture.
Paroxysmal Nocturnal Dyspnea (PND)
 refers to acute episodes of severe shortness
of breath and coughing that generally occur
at night and awaken the patient from sleep,
usually 1–3 h after the patient retires.
 may be manifest by coughing or wheezing,
possibly because of increased pressure in
the bronchial arteries leading to airway
compression, along with interstitial
pulmonary edema leading to increased
airway resistance
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often have persistent coughing and
wheezing even after they have
assumed the upright position.
Cardiac asthma is closely related to
PND, is characterized by wheezing
secondary to bronchospasm, and must
be differentiated from primary asthma
and pulmonary causes of wheezing.
Cheyne-Stokes Respiration
 Also referred to as periodic respiration
or cyclic respiration
 common in advanced HF and is usually
associated with low cardiac output.

caused by a diminished sensitivity of the
respiratory center to arterial PCO2.
– There is an apneic phase, during which the
arterial PO2 falls and the arterial PCO2 rises.
– These changes in the arterial blood gas content
stimulate the depressed respiratory center,
resulting in hyperventilation and hypocapnia,
followed in turn by recurrence of apnea.

may be perceived by the patient or the
patient's family as severe dyspnea or as a
transient cessation of breathing.
NYHA Classification
Physical Examination
General Appearance and Vital Signs
 mild or moderately severe HF- no
distress at rest, except for feeling
uncomfortable when lying flat for
more than a few minutes.
 severe HF- patient sits upright, may
have labored breathing, and may not
be able to finish a sentence because of
shortness of breath.

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Systolic blood pressure may be normal
or high in early HF, but it is generally
reduced in advanced HF because of
severe LV dysfunction
Pulse pressure may be diminished,
reflecting a reduction in stroke
volume.
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Sinus tachycardia is a nonspecific sign
caused by increased adrenergic
activity.
Peripheral vasoconstriction leading to
cool peripheral extremities and
cyanosis of the lips and nail beds is
also caused by excessive adrenergic
activity.
Jugular Venous Pulsation (JVP)


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provides an estimation of right atrial
pressure
best appreciated with the patient lying
recumbent, with the head tilted at 45°
quantified in centimeters of water (normal
8 cm) by estimating the height of the
venous column of blood above the sternal
angle in cm and then adding 5 cm

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In the early stages of HF, the venous
pressure may be normal at rest but
may become abnormally elevated with
sustained (~1 min) pressure on the
abdomen (positive abdominojugular
reflux).
Giant v waves indicate the presence of
tricuspid regurgitation.
Pulmonary Examination
 rales - transudation of fluid from the
intravascular space into the alveoli.
 pulmonary edema - rales over both
lung fields and may be accompanied
by expiratory wheezing (cardiac
asthma).

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rales become specific for HF if without
concommitant pulmonary disease
rales are frequently absent in patients
with chronic HF, even when LV filling
pressures are elevated, because of
increased lymphatic drainage of
alveolar fluid.

Pleural effusions result from the
elevation of pleural capillary pressure
and the resulting transudation of fluid
into the pleural cavities.
– occur most commonly with biventricular
failure because pleural veins drain into
both the systemic and pulmonary veins
– often bilateral in HF, when unilateral they
occur more frequently in the right pleural
space.
Cardiac Examination
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although essential, frequently does not
provide useful information about the
severity of HF.
If cardiomegaly is present, PMI is usually
displaced below the fifth intercostal space
and/or lateral to the midclavicular line, and
the impulse is palpable over two
interspaces.
Sustained or prolonged left parasternal lift
for severe hypertrophy

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An S3 (or protodiastolic gallop) most
commonly present if with volume
overload
A fourth heart sound (S4) is not a
specific indicator of HF but is usually
present in patients with diastolic
dysfunction
Abdomen
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Hepatomegaly
Ascites
– a late sign
– due increased pressure in the hepatic
veins and the veins draining the
peritoneum.
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Jaundice -impairment of hepatic
function due to hepatic congestion and
hepatocellular hypoxia, and is
associated with elevations of both
direct and indirect bilirubin.
Extremities
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Peripheral edema
– cardinal manifestation but nonspecific
and usually absent in patients who have
been treated adequately with diuretics.
– usually symmetric and dependent in HF
and occurs predominantly in the ankles
and pretibial region in ambulatory
patients
– in bedridden patients presacral edema
and the edema of scrotum.
– Long-standing edema may be associated
with indurated and pigmented skin.
Cardiac Cachexia
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severe chronic HF - marked weight loss and
cachexia.
Multifactorial
– elevation of the resting metabolic rate
– anorexia, nausea, and vomiting due to
congestive hepatomegaly and abdominal fullness
– elevation of circulating concentrations of
cytokines such as TNF
– impairment of intestinal absorption due to
congestion of the intestinal veins.

suggests a poor overall prognosis.
Diagnosis
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relatively straightforward if with classic
signs and symptoms of HF but signs
and symptoms of HF are neither
specific nor sensitive.
high index of suspicion
additional laboratory testing
sometimes indicated
Routine Laboratory Testing
 CBC, electrolytes, blood urea nitrogen,
serum creatinine, hepatic enzymes,
urinalysis
 In selected patients
– FBS or OGTT
– fasting lipid panel
– thyroid-stimulating function tests
Electrocardiogram (ECG)
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assess cardiac rhythm
determine the presence of LV
hypertrophy or a prior MI (presence or
absence of Q waves)
determine QRS width to ascertain
whether the patient may benefit from
resychronization therapy
Chest X-Ray
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cardiac size and shape
state of the pulmonary vasculature
may identify noncardiac causes of the
patient's symptoms
Assessment of LV Function

2-D echocardiogram/Doppler
– provide a semiquantitative assessment of
LV size and function as well as the
presence or absence of valvular and/or
regional wall motion abnormalities
(indicative of a prior MI).
– Presence of chamber enlargement and
abnormalities of LV diastolic filling
– Assessment of RV size and pulmonary
pressures, which are critical in the
evaluation and management of cor
pulmonale

MRI also provides a comprehensive
analysis of cardiac anatomy and
function and is now the gold standard
for assessing LV mass and volumes.


The most useful index of LV function is
the EF (stroke volume divided by enddiastolic volume).
EF has limitations as a true measure of
contractility as influenced by
alterations in afterload and/or preload.
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
Normal systolic function = EF of >=
50%
Depressed systolic function = EF
<50%
Biomarkers
 B-type natriuretic peptide (BNP) and Nterminal pro-BNP
– released from the failing heart and are relatively
sensitive markers for the presence of HF with
depressed EF
– also elevated in HF patients with a preserved EF
to a lesser degree.
– increase with age and renal impairment, are
more elevated in women, and can be elevated in
right HF from any cause.
– falsely low in obese patients and may
normalize in some patients following
appropriate treatment.
– A normal concentration of natriuretic
peptides in an untreated patient is
extremely useful for excluding the
diagnosis of HF.

troponin T and I, CRF, TNF receptors, and
uric acid, may be elevated in HF and
provide important prognostic information
Exercise Testing

Treadmill or bicycle exercise testing is
not routinely advocated for patients
with HF, but either is useful for
assessing the need for cardiac
transplantation in patients with
advanced HF
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A peak oxygen uptake (VO2) <14
mL/kg per min is associated with a
relatively poor prognosis.
– Patients with a VO2 <14 mL/kg per min
have been shown, in general, to have
better survival when transplanted than
when treated medically
Differential Diagnosis

HF resembles but should be
distinguished from
– (1) conditions in which there is circulatory
congestion secondary to abnormal salt
and water retention but in which there is
no disturbance of cardiac structure or
function (e.g., renal failure)
– (2) noncardiac causes of pulmonary
edema (e.g., acute respiratory distress
syndrome).

Differentiating the dyspnea that arises
from cardiac and pulmonary causes
– noninvasive cardiac imaging, biomarkers,
pulmonary function testing, and chest xray may be useful.
– A very low BNP or N-terminal pro-BNP
may be helpful in excluding a cardiac
cause of dyspnea in this setting


Ankle edema may arise secondary to
varicose veins, obesity, renal disease,
or gravitational effects.
When HF develops in patients with a
preserved EF, it may be difficult to
determine the relative contribution of
HF to the dyspnea that occurs in
chronic lung disease and/or obesity.
Treatment
Strategies to prevent/reverse HF progression

HF should be viewed as a continuum that is
comprised of four interrelated stages.
– Stage A: patients who are at high risk for
developing HF but without structural heart
disease or symptoms of HF (e.g., patients with
diabetes mellitus or hypertension).
– Stage B: patients who have structural heart
disease but without symptoms of HF (e.g.,
patients with a previous MI and asymptomatic
LV dysfunction).
– Stage C: patients who have structural
heart disease and have developed
symptoms of HF (e.g., patients with a
previous MI with dyspnea and fatigue)
– Stage D: patients with refractory HF
requiring special interventions (e.g.,
patients with refractory HF who are
awaiting cardiac transplantation).

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stage A: treat preventable cause
Stages B and C: treat with drugs that
prevent disease progression (e.g., ACE
inhibitors and beta blockers)
Stage D: symptomatic management of
patients
Defining an Appropriate Therapeutic
Strategy for Chronic HF


Therapy of patients with HF depends
on NYHA Classification
class I (LV systolic dysfunction but remain
asymptomatic)
– slow disease progression by blocking
neurohormonal systems that lead to
cardiac remodeling

Class II–IV
– alleviate fluid retention, lessen disability,
and reduce the risk of further disease
progression and death.
– Combination of diuretics (to control salt
and water retention) with neurohormonal
interventions (to minimize cardiac
remodeling).
Management of HF with Depressed
Ejection Fraction (<40%)
General Measures
 screen for and treat comorbidities such
as hypertension, CAD, diabetes
mellitus, anemia, and sleep-disordered
breathing.
 stop smoking and to limit alcohol
consumption to two standard drinks
per day in men or one per day in
women

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Extremes of temperature and heavy
physical exertion should be avoided.
Avoidance of drugs are known to
make HF worse
– NSAID and Cox2 are not recommended in
patients with chronic HF

increase risk of renal failure and fluid
retention which is markedly increased in the
presence of reduced renal function or ACE
inhibitor therapy.

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Flu and pneumococcal immunization to
prevent respiratory infections
educate the patient and family about
HF, the importance of proper diet, and
compliance with meds
Out-pt care in HF clinics with
advanced disease
Activity
 heavy physical labor is not recommended
 routine modest exercise has been shown to
be beneficial in patients with NYHA class I–
III HF.
 euvolemic patients, regular isotonic
exercise such as walking or riding a
stationary bicycle ergometer as tolerated
Diet
 Dietary restriction of sodium (2–3 g
daily)
 Further restriction (<2 g daily) may be
considered in moderate to severe HF.

Fluid restriction (<2L/day) only if
hyponatremia (<130 meq/L) or for
those unresponsive to high doses of
diuretics and sodium restriction


Caloric supplementation is
recommended for patients with
advanced HF and unintentional weight
loss or cardiac cachexia
use of dietary supplements
("nutriceuticals") should be avoided,
no proven benefit
Drugs
Table 227-4 Drugs for treatment of heart failure (EF<40%)
Diuretics
 restore and maintain normal volume
status in patients with congestive
symptoms or signs of elevated filling
pressures

Furosemide, torsemide, and
bumetanide act at the loop of Henle
(loop diuretics) by reversibly inhibiting
the reabsorption of Na+, K+, and Cl–
in the thick ascending limb of Henle's
loop
– generally required to restore normal
volume status in patients with HF

thiazides and metolazone reduce the
reabsorption of Na+ and Cl– in the
first half of the distal convoluted
tubule
– Metolazone: potent diuretic used in pts
with CRI

potassium-sparing diuretics such as
spironolactone act at the level of the
collecting duct.
Adverse Effects
 potential to produce electrolyte and
volume depletion, as well as
worsening azotemia.
 may lead to worsening neurohormonal
activation and disease progression.

alterations in potassium homeostasis
which increases the risk of lifethreatening arrhythmias.
– loop- and thiazide-type diuretics lead to
hypokalemia
– spironolactone, eplerenone, and
triamterene lead to hyperkalemia
Preventing Disease Progression

cornerstones of modern therapy for HF
with a depressed EF
– ACE inhibitors: interferes with RAAS
activation
– Beta blockers: interferes with excessive
adrenergic nervous system
ACE-inhibitors

should be used in symptomatic and asymptomatic patients
with a depressed EF (<40%)

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interfere with RAAS by inhibiting the enzyme that is
responsible for the conversion of angiotensin I to angiotensin
II.
inhibit kininase II, they may lead to the upregulation of
bradykinin, which may further enhance the beneficial effects
of angiotensin suppression.
stabilize LV remodeling, improve symptoms, reduce
hospitalization, and prolong life.
Caveats
 optimize the dose of diuretic before starting
the ACE inhibitor
 reduce the dose of diuretic during the
initiation of ACE inhibition in order to
prevent symptomatic hypotension.
 ACE inhibitors should be initiated in low
doses, followed by gradual increments if the
lower doses have been well tolerated until
similar to effective dose in clinical trial.
Adverse Effects
 Hypotension and mild azotemia
 Hyperkalemia
 nonproductive cough related to kinin
production(10–15% of patients) and
angioedema (1% of patients)
– May use ARB or combination hydralazine
and nitrates
ACEI vs. Placebo
Angiotensin Receptor Blockers
 well tolerated in patients who are intolerant
of ACE inhibitors because of cough, skin
rash, and angioedema.
 used in symptomatic and asymptomatic
patients with an EF <40% who are ACEintolerant for reasons other than
hyperkalemia or renal insufficiency
 block the effects of angiotensin II on the
angiotensin type 1 receptor.


Some clinical trials have demonstrated
a therapeutic benefit for the addition
of ARB to an ACE inhibitor in patients
with chronic HF.
Adverse Effects
– symptomatic hypotension, azotemia, and
hyperkalemia
B-Adrenergic Receptor Blockers
 represents a major advance in the
treatment of patients with a depressed EF
(<40%)
 interfere with the harmful effects of
sustained activation of the adrenergic
nervous system by competitively
antagonizing one or more adrenergic
receptors ( a1, B1, and B 2)
 When given in concert with ACE inhibitors it
reverse the process of LV remodeling,
improve patient symptoms, prevent
hospitalization, and prolong life.

Adverse Effects
– bradycardia and/or exacerbate heart
block.
– not recommended for patients who have
asthma with active bronchospasm.
Metaanalysis of Beta blockers on
mortality in HF with depressed EF
Aldosterone Antagonists
 drugs that block the effects of aldosterone
(spironolactone or eplerenone)
 recommended for patients with NYHA class IV or
class III (previously class IV) HF who have a
depressed EF (<35%) and who are receiving
standard therapy, including diuretics, ACE
inhibitors, and beta blockers.
 Adverse Effects
– Hyperkalemia
– Painful gynecomastia may develop in 10–15% of patients
who use spironolactone, in which case eplerenone may be
substituted.
Digoxin


symptomatic LV systolic dysfunction
who have concomitant atrial fibrillation
should be considered for patients who
have signs or symptoms of HF while
receiving standard therapy, including
ACE inhibitors and beta blockers.
Anticoagulation and Antiplatelet Therapy
 increased risk for arterial or venous
thromboembolic events.
– Depressed LV function which increase risk
for thrombus formation
– Atrial fibrillation
– Use of warfarin to target INR 2-3

Aspirin is recommended in ischemic
heart disease for the prevention of MI
and death.
– lower doses of aspirin (75 or 81 mg) may
be preferable because of the concern of
worsening of HF at higher doses.
Management of Cardiac Arrhythmias
 Atrial fibrillation occurs in 15–30% of
patients with HF and is a frequent cause of
cardiac decompensation.
– Amiodarone is the preferred drug for restoring
and maintaining sinus rhythm, and it may
improve the success of electrical cardioversion in
patients with HF.


hyperthyroidism, hypothyroidism, pulmonary fibrosis,
and hepatitis
Implantable cardiac defibrillators
– highly effective in treating recurrences of
sustained ventricular tachycardia and/or
ventricular fibrillation
Device Therapy
 Cardiac Resynchronization
 Implantable Cardiac Defibrillators
Acute Heart Failure
therapeutic goals
(1) stabilize the hemodynamic derangements
that provoked the symptoms responsible for
the hospitalization
(2) identify and treat the reversible factors
that precipitated decompensation
(3) reestablish an effective outpatient medical
regimen that will prevent disease
progression and relapse
Pharmacologic
Management of Acute HF
1.
2.
3.
Vasodilators
Inotropic agents
Vasoconstrictors
Drugs for Treatment of Acute HF
Planning for Hospital Discharge
 Patient education
– focus on salt and fluid status
– obtaining daily weights, in addition to
medication schedules.
– Criteria for discharge should include at least 24 h
of stable fluid status, blood pressure, and renal
function on the oral regimen planned for home.
– Patients should be free of dyspnea or
symptomatic hypotension while at rest, washing,
and walking on the ward.
Cor pulmonale


often referred to as pulmonary heart
disease,
dilation and hypertrophy of the right
ventricle (RV) in response to diseases
of the pulmonary vasculature and/or
lung parenchyma.
Etiology of Chronic Cor Pulmonale
Pathophysiology and
Basic Mechanisms

common pathophysiologic mechanism
– pulmonary hypertension that is sufficient
to lead to RV dilation, with or wthout the
development of concomitant RV
hypertrophy.
Clinical Manifestations
Symptoms
 Dyspnea
– increased work of breathing secondary to
changes in elastic recoil of the lung (fibrosing
lung diseases) or altered respiratory mechanics


Orthopnea and paroxysmal nocturnal
dyspnea are rarely symptoms of isolated
right HF.
Tussive or effort-related syncope
– severe pulmonary hypertension because of the
inability of the RV to deliver blood adequately to
the left side of the heart.


abdominal pain and ascites
Lower-extremity edema
– due to neurohormonal activation, elevated RV
filling pressures, or increased levels of carbon
dioxide and hypoxia, which can lead to
peripheral vasodilation and edema formation.
Signs
 tachypnea, elevated jugular venous
pressures, hepatomegaly, and lowerextremity edema
 prominent v waves in the jugular venous
pulse as a result of tricuspid regurgitation.
 RV heave palpable along the left sternal
border or in the epigastrium.
 systolic pulmonary ejection click may be
audible to the left of the upper sternum.


increase in intensity of the holosystolic
murmur of tricuspid regurgitation with
inspiration ("Carvallo's sign")
Cyanosis due to low cardiac output
with systemic vasoconstriction and
ventilation-perfusion mismatches in
the lung.
Diagnosis

The most common cause is left heart failure
– evaluate the patient for LV systolic and diastolic dysfunction.

ECG
–

P pulmonale, right axis deviation, RV hypertrophy.
Chest x-ray
– enlargement of the main pulmonary artery, hilar vessels, and the
descending right pulmonary artery.

Spiral CT scans of the chest
– acute thromboembolic disease

high-resolution CT scan of the chest
– diagnose emphysema and interstitial lung disease

2D-echocardiogram
– measuring RV thickness and chamber dimensions as well as the anatomy
of the pulmonary and tricuspid valves
– interventricular septum may move paradoxically during systole in the
presence of pulmonary hypertension
– Doppler echocardiography can be used to assess pulmonary artery
pressures

MRI
– assessing RV structure and function particularly in patients who are
difficult to image with 2-D echocardiography because of severe lung
disease

Right-heart catheterization
– confirm diagnosis of pulmonary hypertension and for excluding elevated
left-heart pressures (measured as the PCWP) as a cause for right heart
failure.

BNP and N-terminal BNP levels
– elevated in patients with cor pulmonale secondary to RV stretch and may
be dramatically elevated in acute pulmonary embolism.
Treatment


target the underlying pulmonary disease, since this
will lead to a decrease in pulmonary vascular
resistance and relieve the pressure overload on the
RV
General principles of treatment
– include decreasing the work of breathing using
noninvasive mechanical ventilation
– Bronchodilation
– steroids, as well as treating any underlying infection
– Adequate oxygenation (oxygen saturation 90–92%) will
also decrease pulmonary vascular resistance and reduce
the demands on the RV.
– Patients should be transfused if they are anemic, and a
phlebotomy should be performed to reduce pulmonary
artery pressure if the hematocrit exceeds 65%.

Diuretics are effective in the treatment of
RV failure, and the indications for their use
are similar to those for chronic HF
– caveat of chronic diuretic use is that they may
lead to contraction alkalosis and worsening
hypercapnea.

Digoxin is of uncertain benefit in the
treatment of cor pulmonale and may lead to
arrhythmias in the setting of tissue hypoxia
and acidosis.
– Given at low doses and monitored carefully