CONGESTIVE CARDIAC FAILUREAnita. F. LopesPrincipal, Uday Ger School of NursingCardinal Gracias Memorial Hospital Trust

OBJECTIVESThe group is able to : Revise the basic terms. explain the meaning and define CCF. Identify the high risk factors of CCF Identify the causes of CCF Describe the types of CCF Differentiate between Left sided and Right sided

heart failure Identify and co-relate the pathophysiology of CCF List the necessary investigations Carry out the pharmacologic interventions as

prescribed Carry out the Nursing management Provide home-health care education to patient and

significant others

BASICS: Cardiac output: amount of blood pumped per

minute. CO= HR x SV (amount of blood pumped out of the ventricles with each contraction)

Ejection fraction: is the proportion of blood in the heart pumped out of the heart during a single contraction. It is a percentage with normal being between 50 and 75%.

Cardiac Reserve: It is the heart’s ability to increase output in response to stress ( 5 times)

DEFINITION

Heart failure (HF), often used to mean chronic heart failure (CHF), occurs when the heart is unable to pump sufficiently to maintain blood flow to meet the needs of the body

MEANING

Heart failure is a physiological state in which cardiac output is insufficient to meet the needs of the body and lungs. The termed "congestive heart failure" (CHF) is often used as one of the common symptoms is swelling or water retention.

RISK FACTORS Dysrhythmias, especially tachycardia Systemic infections( sepsis) Anemia Thyroid disorders Pulmonary embolism Thiamine deficiency Chronic Pulmonary diseases Medication dose changes Physical or emotional stress Endocarditis, Myocarditis or Pericarditis Fluid retention from medication or salt intake

ETIOLOGY The performance of the heart ( SV) depends

on 4 essential components: Preload: amount of blood present in the

ventricle just before systole Afterload: refers to the amount of resistance

to the ejection of blood from the ventricle Contractility: the force of contraction, is

related to the status of myocardium. Heart rate

COMMON CAUSES The causes of heart failure can be divided

into 3 subgroups: Abnormal loading conditions Abnormal muscle function Conditions or diseases that limit ventricular

filling

CAUSES: ABNORMAL LOADING CONDITIONS

Regurgitation of mitral or tricuspid valve

Hypervolemia Congenital defects

( left to right shunt) VSD ASD PDA

Hypertension Pulmonary Stenosis

or Pulmonic Stenosis.

High Peripheral Vascular resistance

Conditions that increase Preload:

Conditions that increase After load:

CAUSES: ABNORMAL MUSCLE FUNCTIONS MI Myocarditis Cardiomyopathy Ventricular Aneurysm Long term alcohol consumption Coronary Heart disease Metabolic Heart disease Endocrine heart disease

Mitral or tricuspid stenosis. Cardiac tamponade. Constrictive Pericarditis. Hypertrophic obstructive cardiomyopathy.

CAUSES: LIMITED VENTRICULAR FILLING

TYPES OF HEART FAILUREHeart failure is divided into two different types: Heart failure due to reduced ejection fraction

(HFREF) also known as heart failure due to left ventricular systolic dysfunction or systolic heart failure. This occurs with reduced ejection fraction occurs when the ejection fraction is less than 40%.

Heart failure with preserved ejection fraction (HFPEF) also known as diastolic heart failure or heart failure with normal ejection fraction (HFNEF). In diastolic heart failure, the heart muscle contracts well but the ventricle does not fill with blood well in the relaxation phase.

TYPES OF HEART FAILURE Acute decompensated heart failure:  is worsening

or decompensated heart failure, referring to episodes in which a person can be characterized as having a change in heart failure signs and symptoms resulting in a need for urgent therapy or hospitalization

TYPES OF HEART FAILURE Heart failure may also occur in situations of "high

output," (termed "high output cardiac failure") where the ventricular systolic function is normal but the heart cannot deal with an important augmentation of blood volume

PATHOPHYSIOLOGY When cardiac output is not sufficient to meet the

metabolic needs of the body, compensatory mechanisms including neurohormonal responses become activated

These mechanisms help to improve contraction and maintain integrity of the circulation but, if continued lead to abnormal cardiac muscle growth and reconfiguration of the heart ( i.e. remodeling by Amyloidosis in which protein is deposited in the heart muscle, causing it to stiffen )

PATHOPHYSIOLOGY The compensatory responses to decrease the

cardiac output are ventricular dilation, increased sympathetic nervous system stimulation, and activation of Renin-angiotensin mechanism.

1) Ventricular Dilation: Lengthening of the muscle fibers that increase the volume in the heart chambers.

Dilation causes an increase in the preload, thus cardiac output because stretched muscles contracts more forcefully( Starling’s law), however dilation has limits as a compensatory mechanism…slowly become ineffective….this dilated heart requires more oxygen….hypoxia..further reduction in ability to contract.

2)Increased sympathetic nervous system stimulation:

Sympathetic activity produces venous and arteriolar constriction, tachycardia and increased myocardial contractility, all of which work to increase cardiac output and improve delivery of oxygen and nutrients to tissues

This compensatory effect occurs at the cost of increasing peripheral vascular resistance (afterload) and myocardial workload

However in addition, sympathetic stimulation reduces renal blood flow and stimulates the Renin Angiotensin Mechanism

3) Activation of Renin-angiotensin mechanism: When blood flow through renal artery is decreased,

the baroreceptors reflex is stimulated and renin is released in the blood stream.

Renin interacts with angiotensinogen to produce Angiotensin I

Angiotensin I comes in contact with ACE, it gets converted to Angiotensin II ( a potent vasoconstrictor)

This causes arterial vasoconstriction, promotes the release of Nor Epinephrine from sympathetic nerve endings .

This further stimulate the adrenal medulla to severe secrete aldesterone, which enhances sodium and water retention.

Thus stimulation of RAM causes plasma volume to expand and preload to increase.

Once cardiac output is restored , the body produces counterregulatory substances that restore cardiovascular homeostasis.

If underlying pathology is not corrected, prolonged activation of compensatory mechanism eventually leads to changes in the function of the myocardial cell and excess neurohormones are produces.

This process are responsible for the transition from compensated to decompensated heart failure.

At this point heart failure develop because the heart can not maintain adequate circulation.

LV FAILURE Thus when compensatory mechanism fail, the

amount of blood remaining in the left ventricle at the end of diastole increases.

This increase in the residual blood in turn decreases the ventricles capacity to receive blood from left atrium.

The LA has to work harder to eject blood, dilates and hypertrophies. It is unable to receive the full amount of incoming blood from the coronary veins, and the LA pressure increases this leads to pulmonary edema. Thus LVF results.

RV FAILURE The right ventricle because of the increased

pressure in the pulmonary vascular system, must now dilate and hypertrophy to meet it’s increased workload.

It too eventually fails. Engorgement of the venous system then extends

backward to produce congestion in the GI tract, Liver, Viscera, Kidneys, Legs and sacrum…..Edema is the manifestation

Usually RVF follows LVF… but both may occur independently

DECOMPENSATED HEART FAILURE Remodeling: Several structural changes occur in

the ventricle, known as remodeling during decompensated heart failure.

It is due to hypertrophy of the myocardial cells and sustained activation of Neurohormonal compensatory system

When used over time, these responses eventually increase the heart failure by reducing the myocardial contractility, increasing ventricular wall stress and increasing the oxygen demand

Apoptosis: Premature death of Myocardial cells ( programmed cell death)

SIGNS AND SYMPTOMS Heart failure symptoms are traditionally and

somewhat arbitrarily divided into "left" and "right" sided, recognizing that the left and right ventricles of the heart supply different portions of the circulation.

LEFT-SIDED FAILURE

SIGNS AND SYMPTOMS

SIGNS ANDS SYMPTOMS

Three point position: Due to orthopnea the client often assumes “ three point position” , sitting up with both hands on the knees and leaning forward.

Orthopnea develops because the supine position increases the amount of blood returning from the lower extremities to the heart and lung

JUGULAR VEIN DISTENTION

SIGNS AND SYMPTOMS Biventricular failure Dullness of the lung fields to finger percussion

and reduced breath sounds at the bases of the lung may suggest the development of a pleural effusion (fluid collection in between the lung and the chest wall). Though it can occur in isolated left- or right-sided heart failure, it is more common in biventricular failure because pleural veins drain into both the systemic and pulmonary venous systems. When unilateral, effusions are often right sided.

INVESTIGATIONS Echocardiography is commonly used to support a clinical

diagnosis of heart failure. This modality uses ultrasound to determine the stroke

volume (SV, the amount of blood in the heart that exits the ventricles with each beat), the end-diastolic volume (EDV, the total amount of blood at the end of diastole), and the SV in proportion to the EDV, a value known as the ejection fraction (EF). In pediatrics, the shortening fraction is the preferred measure of systolic function. Normally, the EF should be between 50% and 70%; in systolic heart failure, it drops below 40%.

Echocardiography can also identify valvular heart disease and assess the state of the pericardium (the connective tissue sac surrounding the heart). Echocardiography may also aid in deciding what treatments will help the patient, such as medication, insertion of animplantable cardioverter-defibrillator or cardiac resynchronization therapy. Echocardiography can also help determine if acute myocardial ischemia is the precipitating cause, and may manifest as regional wall motion abnormalities on echo.

INVESTIGATIONS ECG An electrocardiogram (ECG/EKG) may be

used to identify arrhythmias, ischemic heart disease, right and left ventricular hypertrophy, and presence of conduction delay or abnormalities (e.g. left bundle branch block). Although these findings are not specific to the diagnosis of heart failure a normal ECG virtually excludes left ventricular systolic dysfunction.

INVESTIGATIONS Chest X-rays are frequently used to aid in the

diagnosis of CHF. In a person who is compensated, this may

show cardiomegaly (visible enlargement of the heart), quantified as the cardiothoracic ratio (proportion of the heart size to the chest). In left ventricular failure, there may be evidence of vascular redistribution ("upper lobe blood diversion" or "cephalization"), Kerley lines, cuffing of the areas around the bronchi, and interstitial edema. Ultrasound of the lung may also be able to detect Kerley lines.

INVESTIGATIONS Blood tests. Blood tests routinely performed include electrolytes (sodium, potassium),

measures of renal function, liver function tests, thyroid function tests, a complete blood count, and often C-reactive protein if infection is suspected. An elevated B-type natriuretic peptide (BNP) is a specific test indicative of heart failure. Additionally, BNP can be used to differentiate between causes of dyspnea due to heart failure from other causes of dyspnea. If myocardial infarction is suspected, various cardiac markers may be used.

According to a meta-analysis comparing BNP and N-terminal pro-BNP (NTproBNP) in the diagnosis of heart failure, BNP is a better indicator for heart failure and left ventricular systolic dysfunction. In groups of symptomatic patients, a diagnostic odds ratio of 27 for BNP compares with a sensitivity of 85% and specificity of 84% in detecting heart failure.

Angiography Heart failure may be the result of coronary artery disease, and its prognosis

depends in part on the ability of the coronary arteries to supply blood to the myocardium (heart muscle). As a result, coronary catheterization may be used to identify possibilities for revascularization through percutaneous coronary intervention or bypass surgery.

Monitoring Various measures are often used to assess the progress of patients being

treated for heart failure. These include fluid balance (calculation of fluid intake and excretion), monitoring body weight (which in the shorter term reflects fluid shifts).

CLASSIFICATION Functional classification generally relies on the

New York Heart Association functional classification. The classes (I-IV) are:

Class I: no limitation is experienced in any activities; there are no symptoms from ordinary activities.

Class II: slight, mild limitation of activity; the patient is comfortable at rest or with mild exertion.

Class III: marked limitation of any activity; the patient is comfortable only at rest.

Class IV: any physical activity brings on discomfort and symptoms occur at rest.

STAGES OF HEART FAILURE In its 2001 guidelines the American College of

Cardiology/American Heart Association working group introduced four stages of heart failure:

Stage A: Patients at high risk for developing HF in the future but no functional or structural heart disorder.

Stage B: a structural heart disorder but no symptoms at any stage.

Stage C: previous or current symptoms of heart failure in the context of an underlying structural heart problem, but managed with medical treatment.

Stage D: advanced disease requiring hospital-based support, a heart transplant or palliative care.

PHARMACOLOGIC MANAGEMENT The goal of treatment in those with chronic heart

failure is the prevention of acute decompensation, to counteract the deleterious effects of cardiac remodeling, and to minimize the symptoms.

Angiotensin-converting enzyme (ACE) inhibitors: reduces systolic function

Angiotensin II receptor Blockers: decreases BP/ Decreases systemic vascular resistance and improves cardiac output

Hydralazine and Isosorbide Dinitrate: Nitrates causes Venous dilation which reduces the amount of blood return to the heart and lowers preload and Hydralazine lowers systemic vascular resistance and left ventricular afterload ( This is given when ACE inhibitors are not tolerated)

PHARMACOLOGIC MANAGEMENT Beta-Blockers: Constant stimulation of the

Sympathetic Nervous system Diuretics: removes excess extracellular fluid by

increasing the rate of urine produced in patients with s/s of fluid overload

Digitalis: Increases the force of myocardial contraction and slows the conduction through AV node: Improves contractility, increases LV output which also results in enhanced diuresis.

Calcium Channel Blockers: CI in pts with systolic dysfuntion…can be used with patients with diastolic dysfunction: causes vasodilation, reduces systemic vascular resistance

Dobutamine Supplemental Oxygen Nutrition: low sodium diet

2-3gms/day

SURGICAL MANAGEMENT Heart transplantation Cardiomyoplasty: Procedure involves wrapping the

latissimus dorsi muscle around the heart and electrostimulating it in synchrony with ventricular systole

Immediate postoperative care is similar to that of any cardiac surgery

NURSING MANAGEMENT: Decreased cardiac output related to heart failure

or Dysrhythmias or both Excess Fluid Volume related to reduced Glomerular

filtration, decreased cardiac output, increased antidiuretic hormone (ADH) and aldesterone production and sodium water retention.

Impaired gas exchange related to fluids in alveoli Risk for activity intolerance related to decreased

cardiac output Risk for impaired skin integrity related to

decreased tissue perfusion and activities. Risk for anxiety related to decreased cardiac

output, hypoxia, diagnosis of heart failure and fear of death .

HOME CARE CONSIDERATIONS Report symptoms of dyspnea/ increased Sob,

Wheezing, sleeping upright with pillow Label all medications Review activity program Restrict sodium (DASH) Dietary approaches to

stoop hypertension Pg. 468 Lippincott Follow up No smoking

BIBLIOGRAPHY Lippincott, Manual of Nsg Practice Joyce M. Black Brunner and Siddharth Wikipedia

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