Presented by: Dave Jay S. Manriquez RN.

CONGESTIVE HEART FAILURE

A state of circulatory congestion produced by myocardial dysfunction MI compromises myocardial function by reducing contractility and

producing abnormal wall motion. The ability of the ventricle to empty lessens, the stroke volume falls,

residual volume increases. Heart failure is the inability of the heart to pump the amount of

oxygenated blood necessary to affect venous return and to meet the metabolic requirements of the body.

GENERAL INCIDENCE RATE

- CHF is present in 2 percent of persons age 40 to 59, more than 5 percent of persons age 60 to 69, and 10 percent of persons age 70 and older.

- Prevalence is at least 25 percent greater among the black population than among the white population.

- Prevalence at each age increased substantially between two periods surveyed nationally: 1976-80 and 1988-91

WORLD HEALTH ORGANIZATION

- More than 22 million people worldwide suffer from congestive heart failure.

INCIDENCE IN THE PHILIPPINES

- Out of the 86,241,697 people in the Philippines, 1,521,912 have Congestive Heart Failure

- CHF is the 6th leading cause of mortality in the Philippines, affecting males more often than females.

TYPES OF CONGESTIVE HEART FAILURE

Right Ventricular Failure, Left Ventricular Failure Because the two ventricles of the heart represent two separate

pumping systems, it is possible for one to fail alone for a short period.

Most heart failure begins with left ventricular failure and progresses to failure of both ventricles

Acute pulmonary edema, a medical emergency, results from left ventricular failure.

If pulmonary edema is not treated, death will occur from suffocation because the client literally drowns in his or her own fluids

Forward Failure, Backward Failure In forward failure, an inadequate output of the affected ventricle

causes decreased perfusion to vital signs. In backward failure, blood backs up behind the affected ventricle,

causing increased pressure in the atrium behind the affected ventricle.

Low Output, High Output In low-output failure, not enough cardiac output is available to

meet the demands of the body. High-output failure occurs when a condition causes the heart to

work harder to meet the demands of the body.

Systolic Failure, Diastolic Failure Systolic failure leads to problems with contraction and ejection of

blood. Diastolic failure leads to problems with the heart relaxing and

filling with blood.

CAUSES OF CONGESTIVE HEART FAILURE

Intrinsic Myocardial Infarction Cardiomyopathy/myocarditis Congenital heart disease Valvular heart defects Percarditis/cardiac tamponade

Extrinsic Systemic hypertension Chronic obstructive pulmonary disease Pulmonary embolism Anemia Thyrotoxicosis Metabolic/respiratory acidosis Blood volume excess/polycythemia Drug toxicity Cardiac dysrhythmias

Metabolic diseases

PATHOPHYSIOLOGY (see separate page for pathophysiology)

Congestive Heart Failure Left-sided CHF Right-sided CHF

SIGNS AND SYMPTOMS OF CONGESTIVE HEART FAILURE

Comparison of Left and Right CHFLeft-sided Congestive Heart Failure Right-sided Congestive Heart Failure

Signs of pulmonary congestion

Dyspnea Tachypnea Crackles in

the lungs Dry, hacking

cough Paroxysmal

nocturnal dyspnea Increased BP

(from fluid volume excess)

Dependent edema (legs and sacrum)

Jugular vein distention Abdominal distention Hepatomegaly Splenomegaly Anorexia and nausea Nocturnal diuresis Swelling of the fingers and

hands Increased BP (from fluid

volume excess)

*** Assessment Findings of Acute Pulmonary Edema Severe dyspnea and orthopnea Pallor Tachycardia Expectoration of large amounts of blood-tinged, frothy sputum Wheezing and crackles on auscultation Bubbling respirations Acute anxiety, apprehension, restlessness Profuse sweating Cold, clammy skin Cyanosis Nasal flaring Use of accessory breathing muscles Tachypnea Hypocapnia, evidenced by muscle cramps, weakness, dizziness and

paresthesias

COLLABORATIVE MANAGEMENT

Medications Digitalis Therapy

Major therapy for CHF Has positive inotropic (strengthens force of cardiac

contractility) and negative chronotropic effects (decreases heart rate)

DOC: Lanoxin (Digoxin) Antidote for Toxicity: Digibind Nursing Responsibilities

Assess heart rate before administration; if below 60 bpm or above 120 bpm, withhold the drug.

Monitor serum potassium Assess for signs of Digitalis toxicity

- Bradycardia- GI manifestations (anorexia, nausea, vomiting and

diarrhea)- Dysrhythmias- Altered visual perceptions- In males: gynecomastia, decreased libido and

impotence

Diuretic Therapy To decrease cardiac workload by reducing circulating

volume and thereby reduce preload

Commonly used diuretics: Thiazides: Chlorthiazide (Diuril) Loop diuretics: Furosemide (Lasix) Potassium-Sparing: Spironolactone (Aldactone)

Nursing Responsibilities Assess for signs of hypokalemia when administering

loop and thiazide diuretics. Give potassium supplement and potassium-rich

foods. Administer early in the morning or early in the

afternoon to prevent sleep pattern disturbance related to nocturia.

Vasodilators To decrease afterload by decreasing resistance to

ventricular emptying Commonly used vasodilators:

Nitroprusside (Nipride) Hydralazine (Apresoline) Nifedipine Captopril (Capoten)

Other Drugs Sympathomimetics

Dopamine Dobutamine

TREATMENT

Diet: sodium-restricted diet to prevent fluid excess Activity: balanced program of activity and rest Oxygen Therapy: to increase oxygen supply

NURSING MANAGEMENT

Providing Oxygenation Administer oxygen therapy per nasal cannula at 2-6 LPM as

ordered Evaluate ABG analysis results Semi-Fowler’s or High-Fowler’s position to promote greater lung

expansion

Promoting Rest and Activity Bed rest or limited activity may be necessary during the acute

phase Provide an overbed table close to the patient to allow resting the

head and arms Use pillows for added support when in High-Fowler’s position Administer Diazepam (Valium) 2-10 mg 3-4x a day as ordered to

allay apprehension Gradual ambulation is encouraged to prevent risk of venous

thrombosis and embolism due to prolonged immobility Activities should progress through dangling, sitting up on a chair

and then walking in increased distances under close supervision Assess for signs of activity intolerance (dyspnea, fatigue and

increased pulse rate that does not stabilize readily)

Decreasing Anxiety Allow verbalization of feelings Identify strengths that can be used for coping Learn what can be done to decrease anxiety*** Anxiety causes increased breathlessness which may be perceived by the client as an increase in the severity of the heart failure and this in turn increases anxiety.

Facilitating Fluid Balance Control of sodium intake Administer diuretics and digitalis as prescribed Monitor I and O, weight and V/S Dry phlebotomy (rotating tourniquets)

Providing Skin Care Edematous skin is poorly nourished and susceptible to pressure

sores Change position at frequent intervals Assess the sacral area regularly Use protective devices to prevent pressure sores

Promoting Nutrition Provide bland, low-calorie, low-residue with vitamin supplement

during acute phase Frequent small feedings minimize exertion and reduce

gastroistestinal blood requirements There may be no need to severely restrict sodium intake of the

client who receives diuretics. “No added salt” diet is prescribed. No processed foods in the

diet.

Promoting Elimination Advise to avoid straining at defecation which involves Valsalva

manoeuvre. Administer laxative as ordered Encourage use of bedside commode

Facilitating Learning Teach the client and his family about the disorder and self-care Monitor signs and symptoms of recurring CHF (weight gain, loss

of appetite, dyspnea, orthopnea, edema of the legs, persistent cough and report these to the physician)

Avoid fatigue, balance rest with activity Observe prescribed sodium restrictions SFF rather than 3 large meals a day Take prescribed medications at regular basis Observe regular follow-up care as directed

*** If acute pulmonary edema occurs in the client with CHF, the following are the appropriate management:

High-fowler’s position Morphine Sulfate 10-15mg/IV as ordered to allay anxiety, reduce

preload and afterlaod Oxygen therapy at 40-70% by nasal cannula or face mask

Aminophylline IV to relieve bronchospasm, increase urinary output and increase cardiac output

Rapid digitalization Diuretic therapy Dopamine and Dobutamine Monitor serum potassium. Diuresis may result to hypokalemia.

PROGNOSIS

- The prognosis depends on the patient's age, the severity of the heart failure, the severity of the underlying heart disease and other factors.

- When congestive heart failure develops suddenly and has a treatable underlying cause, patients can sometimes return to normal heart function after treatment.

- With appropriate treatment, even individuals who develop congestive heart failure as a result of long- standing heart disease can often enjoy many years of productive life.

PATHOPHYSIOLOGYOF

CONGESTIVE HEART FAILURE

PATHOPHYSIOLOGY OF LEFT-SIDED CONGESTIVE HEART FAILURE

CAUSES Heart Damage Ventricular Overload Decreased Ventricular Contraction

TachycardiaVentricular Dilatation

Myocardial Hypertrophy

Decreased Cardiac Output

Decreased Renal Perfusion

Increased Sodium Restriction

Increased Osmotic Pressure

Increased ADH

Increased Water Reabsorption

Fluid Overload Edema

CAUSES: MI HPN Aortic Stenosis/ Insufficiency Mitral Stenosis/ Insufficiency

Reduced Myocardial ContractilityIncreased Cardiac WorkloadDecreased Diastolic Filling

Obstruction of Left Atrial Emptying

Increased Left Atrial Pressure

Left-Sided Congestive Heart Failure

Blood damns back into the pulmonary capillary bed

Pressure of blood into the pulmonary capillary bed increases

Fluid shifts into the intra- and interalveolar spaces

Pulmonary Edema

Decreased stroke volume

Decreased tissue perfusion

Increased cellular hypoxia

Signs and symptoms of LSCHF

Decreased blood flow to the

kidneys

Signs and Symptoms of LSCHF: Dyspnea Paroxysmal Nocturnal

Dyspnea Orthopnea Rales/Crackles Moist Cough Blood Tinged Frothy Sputum Wheezing/ Cardiac Asthma Dizziness Syncope Fatigue Weakness Anorexia Hypokalemia Clubbing of Fingers Polycythemia S3S4 Heart Sounds or Pulsus

Alternans

Decreased blood flow to the kidneys

RAAS Stimulation

Vasoconstriction and Reabsorption of Sodium and WaterIncreased ECF Volume

Increased Total Blood Volume

Increased Systemic BP

PATHOPHYSIOLOGYOF

RIGHT-SIDED CONGESTIVE HEART FAILURE

CAUSES: LSCHF Pulmonary Embolism Right Ventricular Infarction Congenital Septal Defects

Reduced Myocardial ContractilityIncreased Cardiac WorkloadDecreased Diastolic Filling

Obstruction of Right Atrial Emptying

Increased Right Atrial Pressure

Right-Sided Congestive Heart Failure

Blood drums back from the RV to RA

Increased Pressure in the Venous Circuit (Venous Back-

up)

Signs and Symptoms of RSCHF

Signs and Symptoms of RSCHF: Neck Vein Engorgement (Jugular

Vein Distention) Hepatomegaly Portal Hypertension leading to

Cardiac Cirrhosis Ascites Peripheral Edema (Pitting/

Dependent) Splenomegaly Jaundice Hemolytic Anemia Internal Hemorrhoids Leg Varicosities Weight Gain S3S4 Heart Sounds Elevated CVP Reading

***The RSCHF which results from pulmonary disorders is called COR PULMONALE.