a brief synopsis of acute decompensated heart failure

A Brief Synopsis of acute decompensated heart failure

Dr. Emad EfatShebin El kom Chest hospital

June 2017

DefinitionAcute 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.

DefinitionCHF 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

Definition1.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

Definition1.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 activityor 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.

Orthopnea

Paroxysmal nocturnal dyspnea

Left-sided heart failure

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

Physical Examination


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.

The Signs And Symptoms



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)

Causes

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

Risk factors

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 embolus6. Physical or environmental stresses7. 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.

InvestigationsLab 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, dilutionalhyponatremia).

InvestigationsImaging 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 consolidationsand air bronchograms ( Bat's wing or butterflypulmonary 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 suspectedcongestive 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

InvestigationsHigh-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 - HRCTStage 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 lowerright 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

Investigations - HRCT2. 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 demonstratessmooth 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 slightlylarger than the bronchus.

Investigations - HRCT3. Fluid in the major or minor fissure produces thickening of the

fissure4. Peribronchovascular interstitial thickening5. ground-glass opacities6. mosaic pattern of attenuation7. pleural effusion8. lymph nodes may be enlarged

congestive heart failure presenting ground-glass opacities and smoothinterlobular septa thickening, a mosaic pattern of attenuation and bilateral pleural effusion

Thickening of the right major fissure from subpleural edema

Investigations - HRCTStage 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 Cardiogenic pulmonary edema presenting consolidations, ground-glass opacities, smooth interlobular septal thickeningand bilateral pleural effusion.

Investigations - HRCTCardiomegaly: 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/CT (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% nonrebreatherfacemask.

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 hemodynamicallystable..

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 adenosinereceptor 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 , Terbutalineas 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

Thank you

a brief synopsis of acute decompensated heart failure

Health & Medicine