A brief synopsis of acute decompensated heart failure

A Brief Synopsis of acute
decompensated heart failure
Dr. Emad Efat
Shebin El kom Chest hospital
June 2017

Definition
Acute decompensated heart failure (ADHF): a common and
potentially fatal cause of acute respiratory distress.
1. The clinical syndrome is characterized by the
development of dyspnea, generally associated with
rapid accumulation of fluid within the lung's interstitial
and alveolar spaces, which is the result of acutely
elevated cardiac filling pressures (cardiogenic
pulmonary edema).
2. ADHF can also present as elevated left ventricular filling
pressures and dyspnea without pulmonary edema.

Definition
CHF can be categorized into:
Systolic versus diastolic
Left-sided versus right –sided
Left lungs
Right peripheral
Acute versus chronic
Acute- MI
Chronic-cardiomyopathy
High output hypermetabolic state

Definition
1.Systolic heart failure: Diagnosed when the ejection
fraction has decreased below the threshold of 55%.
The ejection fraction is a calculation of how much blood
is ejected out of the left ventricle (stroke volume)
divided by the maximum volume remaining in the left
ventricle at the end of diastole
2. Diastolic heart failure:
 This condition occurs when the heart can contract
normally but is stiff, or less compliant
 More common in patients older than 75 years of age,
especially in patients with high blood pressure, and it
is also more common in women.

Definition
1.Left-sided heart failure: Fluid collects in the lungs
makes it more difficult for the airways to expand as a
person inhales. Breathing becomes more difficult and the
person may feel short of breath, particularly with activity
or when lying down.
2.Right-sided heart failure: Fluid begins to collect in the
feet and lower legs (pitting edema). With pitting edema,
a finger pressed on the swollen leg leaves an imprint.
Non-pitting edema is not caused by heart failure. As the
right heart failure worsens, the upper legs swell and
eventually the abdomen collects fluid (ascites). Weight
gain accompanies the fluid retention.

The American College of Cardiology/American Heart
Association stages patients according to the progression of
their heart failure. The stages are as follows:
Stage A: High risk for developing heart failure
– Patient has one or more risk factors for developing heart
failure.
Stage B: Asymptomatic heart failure
– This stage includes patients who have an enlarged or
dysfunctional left ventricle from any cause, but are
asymptomatic.
Stage C: Symptomatic heart failure
– Patient experiences heart failure symptoms shortness of
breath, fatigue, inability to exercise, etc.
Classification

Stage D: Refractory end stage heart failure
– Patient has heart failure symptoms at rest in spite of
medical treatment.
– Cardiac transplantation, mechanical devices, more
aggressive medical therapy, or end of life care may be
necessary.
New York Heart Association's functional classification :
 Class I No limitation of physical activity.
 Class II Slight limitation of physical activity.
 Class III Marked limitation of physical activity.
 Class IV Symptoms occur even at rest; discomfort with
any physical activity.
Classification

Symptoms
 Dyspnea with progressively increasing severity as the
following:
 Exertional dyspnea: The most sensitive symptom
 Orthopnea: dyspnea that develops in the recumbent
position and is relieved with elevation of the head with
pillows.
 Paroxysmal nocturnal dyspnea (PND): sudden awakening
of the patient, after a couple of hours of sleep, with a
feeling of severe anxiety, breathlessness, and suffocation
 Dyspnea at rest
 Acute pulmonary edema
 Cough: Cough that produces pink, frothy sputum is highly
suggestive of congestive heart failure (CHF).
 Wheezing

Symptoms
 Chest pain/pressure
 Palpitations: are the sensation a patient has when the
heart is racing.
 Common non-cardiac signs and symptoms of heart
failure include:
fatigue, weakness
anorexia, nausea, weight loss, bloating
oliguria, nocturia
cerebral symptoms: confusion, memory impairment,
anxiety, headaches, insomnia, nightmares.

Physical Examination
 Cardiac cachexia
 The pulse may be weak, rapid, and thread
 Systolic arterial pressure may be reduced
 The proportional pulse pressure (pulse pressure/systolic
pressure) may be markedly reduced
 Fever may be present
 Diaphoresis, pallor, peripheral cyanosis and coldness of
the extremities
 Rales heard over the lung bases
 With acute pulmonary edema, rales are frequently
accompanied by wheezing.

The Signs And Symptoms

 Predominant Right-Sided Heart Failure:
 Jugular venous distention
 Kussmaul sign: Increase jugular venous pressure with
respiration
 Hepatojugular reflux is the distention of the jugular
vein induced by applying manual pressure over the
liver
 Hydrothorax: usually bilateral, or on the right side
 Congestive hepatomegaly and ascites.
 Peripheral edema
 Edema may be severe (anasarca) in severe right heart
failure.

Hepatojugular reflux
Pitting edema

 Cardiac findings:
 Protodiastolic (S3) gallop
 Cardiomegaly: Notable exceptions include heart failure from
acute MI, constrictive pericarditis, restrictive
cardiomyopathy, valve or chordae tendineae rupture, or
heart failure due to tachyarrhythmias or bradyarrhythmias.
 Pulsus alternans (alternation of 1 strong and 1 weak beat)
 Accentuation of P2 heart sound in pulmonary arterial
hypertension
 Mitral and tricuspid regurgitation murmurs: due to
ventricular dilatation.

Causes
 The most common cause is coronary artery disease,
 Hypertension
 Valvular heart disease
 Congenital heart disease
 Cardiomyopathies
 Myocarditis
 Infectious endocarditis.
 Prolonged, serious arrhythmias
 Toxic exposures, such as alcohol or cocaine
 Endocrine disorders (including thyroid disorders)
 Exposures (such as radiation or chemotherapy)

Risk factors
 Age
 Hypertension
 Physical inactivity
 Diabetes
 Obesity
 Smoking
 Metabolic syndrome
 Enlargement of the left
ventricle
 Infection of the heart
muscle (usually viral)
 Pheochromocytoma
 Thyroid disease
 Valvular heart disease
 familial heart disease
 Coronary artery disease
 Dyslipidemia
 Alcohol use
 Substance abuse
 Prior heart attack
 History of
chemotherapy/radiation
to the chest
 Sleep disorders
 Collagen vascular
disease, rheumatic fever

Congestive heart failure may be exacerbated by:
1. lifestyle habits:
 Unhealthy habits, such as smoking and excessive use of alcohol
 Obesity and lack of exercise
 High salt intake, which may cause more fluid retention
 Noncompliance with medications and other therapies
2. Cardiac ischemia
3. Dysrhythmias
4. Cardiac or extracardiac infection
5. Pulmonary embolus
6. Physical or environmental stresses
7. Iatrogenic volume overload.
8. Pregnancy
9. Hyperthyroidism
Precipitating factors

 Acute Respiratory Distress Syndrome
 Altitude Illness - Pulmonary Syndromes
 Anaphylaxis
 Chronic Obstructive Pulmonary Disease and Emphysema
 Anemia
 Acute Bronchitis
 Hyperventilation Syndrome
 Myopathies
 Pericarditis and Cardiac Tamponade
 Pneumonia
 Pneumothorax and Pneumomediastinum
 Pulmonary Embolism
 Shock, Septic
 Venous Air Embolism
Differentials

Other Problems to be Considered
 The cardiac conditions combined with asthma or
symptoms of chronic obstructive pulmonary disease
(COPD) are difficult clinical challenges.
 The standard of care has been shotgun therapy,
namely treating patients for both congestive heart
failure (CHF) and an acute pulmonary process such as
asthma, with both diuretics and beta-agonists.

Investigations
Lab Studies:
1. Serum levels of beta-natriuretic peptide (BNP) and the
BNP precursor, Pro-BNP:
Serum levels of BNP lower than 100 pg/mL are unlikely
to be from CHF. BNP levels more than 500 pg/mL are
most consistent with CHF.
1. Complete blood count (CBC), which may indicate anemia
or infection as potential causes of heart failure
2. Urinalysis (UA), which may reveal proteinuria, which is
associated with cardiovascular disease
3. Serum electrolyte levels, which may be abnormal owing
to causes such as fluid retention or renal dysfunction
4. Blood urea nitrogen (BUN) and creatinine levels, which
may indicate decreased renal blood flow

Investigations
Lab Studies:
5. Fasting blood glucose levels, because elevated levels
indicate a significantly increased risk for heart failure
(diabetic and nondiabetic patients)
6. Elevated alanine aminotransferase (ALT), aspartate
aminotransferase (AST), or bilirubin levels, which is
suggestive of a congestive hepatopathy.
7. Cardiac enzymes and other serum markers for ischemia
or infarction may also be useful.
8. ABG levels may be of benefit (i.e. evaluation of
hypoxemia, Hypercapnia, acidosis, dilutional
hyponatremia).

Investigations
Imaging Studies:
Chest radiography:
– Chest radiography is the most useful tool.
– Cardiomegaly with a cardiothoracic ratio greater than 50%.
– Pleural effusions may be present bilaterally or if they are
unilateral more commonly observed on the right.
– Early CHF may manifest as cephalization of pulmonary vessels,
generally reflecting a pulmonary capillary wedge pressure
(PCWP) of 12-18 mm Hg. As the interstitial fluid accumulates,
more advanced CHF may be demonstrated by Kerley B lines
(PCWP is 18-25 mm Hg).
– Pulmonary edema is observed as perihilar infiltrates often in
the classic butterfly pattern, reflecting a PCWP of more than 25
mm Hg.

Stage I CHF - Redistribution
 Redistribution of the pulmonary veins. This is know as
cephalization (blue arrow) because the pulmonary veins
of the superior zone dilate due to increased pressure.
 An increase in width of the vascular pedicle (red arrows)
Cardiogenic pulmonary edema

The vascular pedicle is bordered on the right by the
superior vena cava and on the left by the left subclavian
artery origin

Stage II CHF - Interstitial edema Characterized by:
1. Kerley’s A lines: extend radially from the hilum to the
upper lobes; represent thickening of the interlobular
septa that contain lymphatic connections.

2. Kerley’s B lines are short horizontal lines situated
perpendicularly to the pleural surface at the lung base;
they represent edema of the interlobular septa.

3. Thickening of the bronchial walls (peribronchial cuffing)
and as loss of definition of these vessels (perihilar haze).

4. Fluid in the major or minor fissure (shown here) produces
thickening of the fissure beyond the pencil-point
thickness it can normally attain

Stage III CHF - Alveolar edema Characterized by:
Alveolar edema with
perihilar consolidations
and air bronchograms
( Bat's wing or butterfly
pulmonary opacities )
(yellow arrows)
pleural fluid (blue arrow)
prominent azygos vein
and increased width of
the vascular pedicle (red
arrow)
an enlarged cardiac silhouette (arrow heads).

 Echocardiography :
 Evaluation of patients with known or suspected
congestive heart failure.
 Establishing the diagnosis of diastolic HF
 Regional wall motion abnormalities.
 Globally depressed or myopathic left ventricular function
 Cardiac tamponade and pericardial constriction.
 Pulmonary embolus.
 Valvular heart disease as mitral or aortic stenosis or
regurgitation.
 Cardiac output (ejection fraction)
 Pulmonary artery and ventricular filling pressures.
Investigations

 ECG:
It is a nonspecific tool but may be useful in diagnosing
concomitant:
 Cardiac ischemia.
 Prior myocardial infarction (MI).
 Cardiac dysrhythmias.
 Chronic hypertension.
 Left ventricular hypertrophy.
Investigations

 Nuclear Imaging
Nuclear imaging can be used in the assessment of heart
function and damage in CHF.
 Angiography:
Cardiac catheterization and coronary angiography are
indicated in the following situations:
CHF caused by systolic dysfunction in association with
angina or regional wall motion abnormalities
Before cardiac transplantation
CHF secondary to post-infarction ventricular aneurysm
or other mechanical complications of MI
Investigations

Investigations
High-resolution computed tomography (HRCT):
Stage I CHF – Redistribution:
 Redistribution of blood flow from the lower to the upper. This is
know as cephalization because the pulmonary veins of the
superior zone dilate due to increased pressure.
 Increased artery-to-bronchus ratio at hilar level (normally they are
equal)
 Cardiomegally
Significant enlargement of
segmental / subsegmental
pulmonary arteries (NB
pulmonary artery-to-
bronchus ratio >1) and
Mosaic attenuation pattern

Investigations - HRCT
Stage II CHF - Interstitial edema Characterized by:
1. Thickened interlobular septa : Septal lines, also known as Kerley
lines, become prominent. They usually occur when pulmonary
capillary wedge pressure reaches 20-25 mmHg.
Smooth septal thickening
(red arrow) in the lower
right lobe, increased
vascular diameter ( yellow
arrow) and bilateral
pleural effusion (black
arrow) in a patient with
congestive heart failure.
Please observe the
aneurysm on the
descending aorta

2. Bronchial wall thickening will also be seen, and is the basis of
peribronchial cuffing seen on chest x-rays.
Interstitial pulmonary edema.
(A) Axial chest CT demonstrates
smooth thickening of
interlobular septae (white
arrow). This is the CT equivalent
of Kerley B lines seen on chest
x-rays. (B) Magnified view from
the RLL in the same patient
demonstrates bronchial wall
thickening (green arrow), which
is the CT equivalent of
peribronchial cuffing seen on
radiographs. Also, note that the
adjacent pulmonary artery
branch (red arrow) is slightly
larger than the bronchus.

3. Fluid in the major or minor fissure produces thickening of the
fissure
4. Peribronchovascular interstitial thickening
5. ground-glass opacities
6. mosaic pattern of attenuation
7. pleural effusion
8. lymph nodes may be enlarged
congestive heart failure presenting
ground-glass opacities and smooth
interlobular septa thickening, a mosaic
pattern of attenuation and bilateral
pleural effusion
Thickening of the right major
fissure from subpleural edema

Stage III CHF - Alveolar edema Characterized by:
 Peribronchial nodules
 Alveolar edema with perihilar consolidations and air
bronchograms ( Bat's wing or butterfly pulmonary opacities )
 Pleural effusion
 An enlarged cardiac silhouette
High-resolution computed
tomography scans, showing
slices acquired at the aortic arch
level, using a pulmonary
window, in a patient with acute
myocardial infarction and
presenting consolidations,
ground-glass opacities, smooth
interlobular septal thickening
and bilateral pleural effusion.

Cardiomegaly:
The heart is enlarged if the cardiothoracic ratio (CTR) is greater than
50% in the axial plane. If the heart is enlarged, check for other signs of
heart failure such as pulmonary oedema, septal lines (or Kerley B
lines), and pleural effusions.
Transverse CTR=T/C
T (superior white arrows)
: the maximum transverse
cardiac diameter. C
(inferior white horizontal
arrows): The transverse
thoracic diameter, would
normally be taken at the
level of the dome of the
left hemidiaphragm

 Central venous catheter (CVC) placement
 Pulmonary artery catheters
 Cardiac catheterization may be necessary for a complete
evaluation and assessment of prognosis.
 Maximal exercise testing with/without respiratory gas
exchange and/or blood oxygen saturation, which
assesses cardiac and pulmonary function with activity
 Screening for sleep-disturbed breathing, which affects
neurohormonal activation
 Holter monitoring, which may reveal arrhythmias or
abnormal electrical activity
Procedures to be done

 Prehospital Care:
1. Begin treatment with the ABCs (Airway, Breathing,
Circulation).
2. Administer supplemental oxygen.
3. Use cardiac monitoring and continuous pulse
oximetry.
4. Obtain intravenous access
5. A prehospital ECG, if available.
6. Provide nitroglycerin sublingual or spray for active
chest pain in the patient without severe hypotension
7. Intravenous furosemide.
Treatment

Treatment
 Emergency Department Care:
1. The ABCs.
2. Administer supplemental oxygen, initially 100% nonrebreather
facemask.
3. Use cardiac monitoring and continuous pulse oximetry.
4. Obtain intravenous access.
5. To reduce venous return, elevate the head of the bed.
6. Start with nitrates and diuretics if patients are hemodynamically
stable..
7. Treat the underlying cause as well, if identified.
8. Eliminate contributing factors when possible.
9. Restrict fluid and sodium.
10. Urine output monitoring (perhaps with urethral catheter
placement)

11. Prophylaxis against venous thromboembolism (deep vein
thrombosis and pulmonary embolism) with low dose
unfractionated heparin or low molecular weight heparin, or
fondaparinux, or by mechanical device (e.g., intermittent
pneumatic compression device)
12. Noninvasive ventilation [NIV]:
Nasal continuous positive airway pressure (CPAP) therapy
and facemask ventilation therapy.
BiPAP therapy may improve ventilation and vital signs more
rapidly than CPAP, a higher incidence of MI associated with
BiPAP has been reported.
13. Patients with respiratory failure who fail to improve with NIV
(within one half to two hours) or do not tolerate or have
contraindications to NIV should be intubated for conventional
mechanical ventilation
Treatment

The airways are kept open using a BiPAP machine.
BiPAP machines are adjusted to dual settings so that
the pressure of the air coming in on inspiration can be
different from the pressure of the air being exhaled.
BiPAP (Bi-level Positive Airway Pressure)

 Diuretics:
First-line therapy, Preload reduction, for acute heart failure.
Given by bolus or continuous infusion and in high or low doses
Generally includes a loop diuretic (ie, furosemide, bumetanide,
torsemide)
In patients with hypertensive heart failure who have mild fluid
retention, thiazide diuretics may be preferred because of their
more persistent antihypertensive effects.
Addition of a second diuretic to potentiate the effects of the loop
diuretic. For patients in whom the diuretic response is
inadequate, intravenous chlorothiazide or oral metolazone or
spironolactone are reasonable choices for a second diuretic.
Other agents, such as vasopressin antagonists and adenosine
receptor blockers, can be used to assist diuretics.
Medication

 Diuretics:
Spironolactone improves survival. In addition, the associated
reduction in collecting tubule sodium reabsorption and
potassium secretion can both enhance the diuresis and minimize
the degree of potassium wasting.
Transition to oral diuretic therapy is made when the patient
reaches a near euvolemic state.
Hemodialysis or ultrafiltration, may be used alternative
strategies, if diuretic resistance occurs.
Ultrafiltration is an effective method of fluid removal that
provides adjustable fluid removal volumes and rates and no effect
on serum electrolytes. However, studies have not found a clinical
benefit over diuretic therapy and it does not preserve renal
function compared to diuresis.
Medication

 Vasodilators:
Vasodilators (eg, nitroprusside, nitroglycerin, or nesiritide) will
decrease preload and/or afterload.
These agents reduce myocardial oxygen demand by lowering
preload and afterload.
Nitroprusside:
 Early vasodilator therapy, in patients with severe hypertension,
acute mitral regurgitation, or acute aortic regurgitation.
It causes balanced arterial and venous dilation like Nesiritide
Nitroglycerin — Nitrates, the most commonly used vasodilators
in ADHF, cause greater venous than arterial vasodilation
Nitrate administration is contraindicated after use of
phosphodiesterase type 5 inhibitors (e.g., sildenafil)
Medication

 Inotropic agents:
Principal inotropic agents include dopamine, dobutamine,
inamrinone (formerly amrinone), milrinone, dopexamine,
and digoxin.
In patients with severe left ventricular systolic dysfunction
and low output syndrome (diminished peripheral perfusion
and endorgan dysfunction), dopamine and dobutamine are
usually used.
Dobutamine is probably the current agent of choice
These agents augment both coronary and renal blood flow.
Patients receiving intravenous inotropes require continuous
blood pressure and cardiac rhythm monitoring.
Medication

 Vasopressors:
In patients with ADHF and marked hypotension
Vasopressors used in this setting include norepinephrine, high
dose dopamine (>5 micrograms/kg/min), and vasopressin
They can be used as a temporizing measure to preserve
systemic blood pressure and endorgan perfusion
They increase afterload and decrease cardiac output
Analgesics:
 Intravenous morphine may be considered in some patients
with acute pulmonary edema as an ungraded
recommendation
 They reduce anxiety and distress associated with dyspnea but
also induce nausea and depress respiratory drive.
Medication

 Digoxin :
Has no role in the emergency management of CHF due to
delayed absorption and diminished efficacy.
Limit use of digoxin to chronic CHF, in which its role has been
well established.
Digoxin is mainly used as an antiarrhythmic to control the rate of
the heart in atrial fibrillation and flutter. In contrast, excessive
digoxin in the blood can cause life threatening arrhythmias.
Although commonly used in the past, digoxin has moved far
down the list of recommended drugs for treatment of heart
failure. It is still considered for patients who are taking ACE
inhibitors, angiotensin receptor blockers (ARBs), beta blockers
and/or diuretics and are still experiencing heart failure
symptoms.
Medication

 ACE inhibitors:
Initiation of therapy For patients who are not already taking an
ACE inhibitor, single agent angiotensin receptor blocker (ARB), or
angiotensin receptor-neprilysin inhibitor, we suggest that such
therapy not be initiated at the time of presentation with an
episode of ADHF.
An oral ACE inhibitor or ARB can usually be started within 24 to 48
hours, once the patient is hemodynamically stable.
Initiation of these therapies known to improve outcomes is
recommended prior to hospital discharge.
Continued therapy For patients who are already taking an ACE
inhibitor, single agent ARB, or ARNI, we suggest that maintenance
of oral therapy be cautiously continued. However, the dose should
be decreased or the drug discontinued if hypotension, worsening
renal function, or hyperkalemia is present.
Medication

 Beta-blockers:
 Beta blockers reduce mortality when used in the long
term management of patients with HF with reduced
ejection fraction,
 but must be used cautiously in patients with
decompensated HF with reduced ejection fraction
because of the potential to worsen acute HF.
 Initiation of therapy prior to discharge is recommended
in stable patients
Medication

Applying the shotgun approach:
 Aerosolized more selective beta-2 agonists , Terbutaline
as well as albuterol, isoetharine, and bitolterol,
decrease tachycardia, dysrhythmias, and cardiac work
while transiently enhancing cardiac function.
 Steroids:
 Not administered by intravenous or oral route, due to
systemic sodium retention and volume expansion,
hypokalemia, and occasional hypertension.
 Inhaled steroids, may be used but because their
delayed onset of action, they remain an area in need
of further study.
Patient with CHF and asthma exacerbations

 Diuretics
 Theophylline and aminophylline:
Limit roles in the acute setting.
They are positive inotropic agents mediated by an increase in
catecholamines, and they dilate coronaries and exert mild
diuretic effects.
they can exacerbate dysrhythmias (eg, multifocal atrial
tachycardia [MAT], ischemia) by increasing cardiac work.
Patient with CHF and asthma exacerbations

Further Inpatient Care:
 Patients presenting with acute symptoms of congestive heart
failure (CHF) or pulmonary edema require hospital admission with
few exceptions:
– gradual onset of shortness of breath
– rapid response to therapy
– oxygen saturation greater than 90%
– No acute coronary syndromes and MI.
 Critical care unit admission for patients who require intubation or
remain with significant respiratory, hemodynamic, and/or
cardiovascular compromise.
Further Outpatient Care:
Patient education with specific instructions regarding dietary
restrictions and compliance with medical therapy.
Follow-up

In/Out Patient Medications:
 ACE inhibitors are indicated in patients with ejection
fractions of 35% or less.
 Digoxin may also be helpful in patients with ejection
fractions of 35% or less.
 Diuretics, such as furosemide, may be helpful
regardless of ejection fraction.
 Carvedilol are indicated as therapy for patients with
diastolic dysfunction or for patients with coronary
insufficiency.
 Calcium channel blockers, Amlodipine are useful in
patients with diastolic dysfunction and heart failure.
Follow-up

1. Electrophysiologic intervention:
 Cardiac resynchronization therapy (CRT)
 Pacemakers
 Implantable cardioverter-defibrillators (ICDs)
2. Revascularization procedures :
 Coronary artery bypass grafting (CABG)
 Percutaneous coronary intervention (PCI)
 Valve replacement or repair
 Ventricular restoration.
3. Mechanical cardiac support:
 Intraaortic balloon pump counterpulsation,
 Extracorporeal membrane oxygenation (ECMO), or
 Short term left ventricular assist devices
Invasive therapies

1. A permanent pacemaker:
A permanent pacemaker is a small device implanted in the chest just
under the collarbone. A pacemaker may be used if the heart's natural
pacemaker (the SA node) is not working properly causing a slow
heart rate or rhythm, or if the electrical pathways are blocked.
Electrophysiologic intervention

1. Cardiac resynchronization therapy (CRT) also known as
biventricular pacing:
It is used for ventricles that don't contract at the same time. This can
worsen heart failure. A biventricular pacemaker paces both ventricles
at the same time, increasing the amount of blood pumped by the
heart.

1. Implantable cardioverter-defibrillators (ICDs):
It looks similar to a pacemaker, though slightly larger. It works very
much like a pacemaker. However, the ICD can send an energy shock
that resets an abnormal heartbeat back to a normal. Many devices
combine a pacemaker and ICD in one unit.

1. Percutaneous coronary intervention (PCI)
The cardiologist places a small, hollow metal (mesh) tube called a
"stent" in the artery to keep it open following a balloon angioplasty.
The stent prevents constriction or closing of the artery during and after
the procedure. Drug-eluding stents are now used. These stents are
coated with medication that helps prevent narrowing of the artery.
Revascularization procedures

2. Coronary artery bypass grafting (CABG):
It is a type of surgery that improves blood flow to the heart. It's used
for people who have severe coronary heart disease (CHD), also called
coronary artery disease. CABG surgery creates new routes around
narrowed and blocked arteries, allowing sufficient blood flow to
deliver oxygen and nutrients to the heart muscle.

3. Valve replacement or repair:
 The ACC/AHA recommends that valve repair or replacement in
patients with hemodynamically significant valvular stenosis or
regurgitation and asymptomatic heart failure should be based on
contemporary guidelines.
 The ACC/AHA indicates that such surgery should be considered for
patients with severe aortic or mitral valve stenosis or regurgitation,
even when ventricular function is impaired.

4. Surgical ventricular restoration:
a | The geometric effects of cardiac dilatation change the normal
elliptical architecture of the heart into b | a spherical form
(myocardial infarction scar shown by the white area). c | Surgical
ventricular restoration reduces ventricular volume and rebuilds
the elliptical shape. In very dilated hearts, the site of patch
placement is either located at the scar or placed just beneath the
aortic valve to rebuild form.

 Mechanical cardiac support:
 For selected patients with severe HF with reduced
ejection fraction (generally with left ventricular ejection
fraction <25 percent) with acute, severe hemodynamic
compromise (cardiogenic pulmonary edema with
cardiogenic shock)
 Nondurable mechanical support is an option as a “bridge
to decision” or “bridge to recovery”
 Mechanical modalities used in this setting include
Intraaortic balloon pump counterpulsation,
extracorporeal membrane oxygenation (ECMO), or short
term left ventricular assist devices
Mechanical cardiac support

Intraaortic balloon pump counterpulsation, during systole, the
balloon is deflated actively (by facilitating the outflow of blood from
the left ventricle to the aorta) and during diastole the balloon inflates
to improve the heart’s perfusion with increased blood flow to the level
of the coronary arteries level, improving overall cardiac function.

ECMO involves an extracorporeal circuit that directly oxygenates and
removes carbon dioxide from the blood using an oxygenator, a gas
exchange device that uses a semipermeable membrane to separate a
blood compartment from a gas compartment.

Ventricular assist devices support the ventricular function of the
heart. The ventricles push blood out of the heart. Depending upon the
site of implantation, it may help to assist the heart with pushing the
blood to the lungs (right side), to the entire body (left side) or
sometimes it may be used in both ventricles (biventricular).

 Selected patients with severe heart failure, debilitating
refractory angina, ventricular arrhythmia, or congenital
heart disease that cannot be controlled despite pharmacologic,
medical device, or alternative surgical therapy should be
evaluated for heart transplantation.
 The patient must be well informed, motivated, and emotionally
stable; have a good social support network; and be capable of
complying with intensive medical treatment.
 Total Artificial Heart (TAH): Despite more than 40 years of
effort, the clinical application of artificial heart technology is still
immature. However, with the approval of the SynCardia device
and with new efforts to create small pumps, TAHs will ultimately
be routine components of heart failure surgery for very sick
patients with heart failure and biventricular failure.
Heart Transplantation

Heart Transplantation
The SynCardia device : Originally used as a permanent
replacement heart, the Total Artificial Heart is currently approved as
a bridge to human heart transplant for transplant-eligible candidates
at risk of imminent death from biventricular failure. It is the world’s
first and only Food and Drug Administration (FDA), Health Canada
and Conformité Européene (CE) approved Total Artificial Heart

 Close monitoring of blood pressure.
 Patient should modify diet as follows:
 Sodium restriction.
 Weight reduction .
 Appropriate fluid restriction .
 Modify activity as follows:
 During severe stage, bed rest with elevation of head
of bed and anti-embolism stockings to help control
leg edema.
 Gradual increase in activity with walking to help
increase strength.
Prevention

 Acute MI
 Cardiogenic shock
 Arrhythmias (most commonly atrial fibrillation)
 Ventricular arrhythmias, such as ventricular
tachycardia,
 Electrolyte disturbances
 Mesenteric insufficiency
 Protein enteropathy
 Digitalis intoxication
Complications

A brief synopsis of acute decompensated heart failure

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