NU 331

Syndrome

of pulmonary or systemic circulatory congestion caused by decreased myocardial contractility, resulting in inadequate CO to meet oxygen requirements of the tissues.
of CHF increases with aging

Incidence

 Primary

causes are disorders producing decreased myocardial contractility:

CAD Valvular heart disease HTN Cardiomyopathy Dysrhythmias Cor pulmonale secondary to lung disease Pericarditis

 Heart

Failures hallmarks are vasoconstriction and fluid retention Typically associated with HTN, CAD and MI, although other diseases and states can lead to heart failure. Characterized by ventricular dysfunction
Increased

incidences in recent years because of advances in medicine, the aging of America, and survival rates after cardiac events.

 Dysfunction

of either the systolic or diastolic functioning of the heart:

Systolic failure: inability to pump blood, ventricles can not contract, left ventricle can not get enough pressure to push blood through the aorta Diastolic failure: inability of ventricles to relax and fill, because of stiff ventricles or venous engorgement in periphery or pulmonary system

 Left:

impaired pumping of the left side, with backup in to pulmonary circulation. Right: impaired pumping of the right side, with backup of blood leading to congestion and elevated pressure in the systemic veins & capillaries. Biventricular: inability of both ventricles to pump blood effectively.

 As

cardiac output falls, the body will attempt to compensate

SNS: Sympathetic Nervous System- activates and releases norepinephine and epinephrine, increasing HR, myocardial contractility, and peripheral vasoconstriction (short term solution) Inflammatory Responses: locally

 As

cardiac output fall the body will attempt to compensate (continued)

RAAS: Renin-Angiotension-Aldosterone Systemas blood flow to the kidney decreases, the kidney releases renin (through juxtaslumerular apparatus stimulation) which converts to angiotension to angiotension II which causes the adrenal cortex to release aldosterone, causing sodium and water retention, increasing peripheral vasoconstriction and BP

 As

cardiac output fall the body will attempt to compensate (continued)

ADH: Antidiuretic Hormone- is secreted by the pituitary when low CO causes decreased cerebral perfusion pressure. ADH increases water reabsorption in renal tubules causing water retention and increased blood volume

 As

the body attempts to compensateall these things together, the SNS, RAAS, ADHall cause increased cardiac workload and myocardial dysfunction resulting in abnormal shaped contractile cells and increased ventricular mass. Impaired contractility = less effective pumping

 Two

symptoms commonly seen in the heart with heart failure:

Dilation is enlargement of the heart chambers, This stretch occurs over time, because of the pressure elevation and increased volume.

Frank-Starling Law: degree of stretch is directly related to the force of contraction

Hypertrophy is the increase in the muscle mass of the wall of the myocardium in response to the workload

 Heart

failure usually manifests itself as biventricular failure- although usually one side decompensates and fails first.

Typically manifests itself with pulmonary edema

Alveoli fill with serosanguineous fluid Usually as a result of LVHF, or decreased efficiency of LV Starts with increased RR and decreased PaO2 As it gets worse, interstitial edema occurs, tachypnea occurs, SOB, respiratory acidosis (increase CO2) Anxious, pale, cyanotic, pink frothy sputum, crackles, increased HR, etc

 Stage

A- at risk, but no structural abnormalities, no symptoms Stage B- some structural evidence on EKG (LV hypertrophy), CXR (cardiomegaly) Stage C- symptomatic, structural heart disease Stage D- end-stage heart failure.

Fatigue Dyspnea, orthopnea, and/or paroxysmal nocturnal dyspnea Tachycardia Edema- peripheral, hepatomegaly, ascites

Skin changes

Dusky coloring Cool, damp Shiny, swollen lower extremities without hair Restlessness, memory issues

Behavioral changes

3 lb weight gain in 2 days is potentially problematic

Nocturia

Angina pain Weight changes

Poor diet Renal failure Hepatomegaly

 Congestion

occurs primarily in the lungs from back up of blood into the pulmonary veins and capillaries because of left ventricular pump failure. Blood backs up in pulmonary bed, causing increased hydrostatic pressure and fluid accumulation in the lungs. Blood flow is decreased to other vital organs (brain, kidneys, etc)

 Assessment

findings:

Dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea Moist crackles on auscultation Frothy blood tinged sputum (pink-tinged sputum) Tachycardia with an s3 and s4 heart sound Pale, cool extremities Peripheral and central cyanosis Decreased peripheral pulses and a delayed capillary refill Decreased urinary output Fatigue Restlessness- possible MS changes and confusion

 Laboratory

and Diagnostics:

CXR Will show cardiomegaly and vascular congestion of lung fields EKG Show hypertrophy or myocardial damage ABGs May show decreased PaO2 and increased PaCO2 Pulse Oximetry may be below 95% Pulmonary artery catheter pressures will reveal: Pulmonary artery and capillary wedge pressures elevated in left sided CHF Elevated central venous pressure in right sided CHF

 Congestion

in systemic circulation from right ventricular pump failure Blood backs up in systemic circulation (right atrium and venous circulation), causing increased hydrostatic pressure and produces peripheral and dependent pitting edema. Usually see venous congestion in kidneys, liver and GI tract as well

 Assessment

Findings:

Dependent pitting edema Anasarca Weight Gain Nausea and vomiting Jugular Vein Distention Liver congestion (hepatomegaly), ascites, or weakness

 Potential

Complication of Heart Failure:

Dysrythmias
Most common is atrial fibrillation Normal depolarization is disrupted with the enlargement of the heart Most common with RV heart failure, lobes of the liver are so congested that the liver can not function correctly- liver cells die and fibrose and cirrhosis develops

Hepatomegaly

 Potential

Complication of Heart Failure: (continued)

Pleural Effusion

From increased pressure in the pleural capillaries Decreased Cardiac Output results in decreased kidney perfusion which leads to insufficiency and failure.

Renal Failure

 Identify

the cause of heart failure, the factors that are aggravating the symptoms, and the current status of the individual to make a plan of care that meets their individual needs. Every case is a little different, most people with HF have other comorbid conditions that have to additionally be considered in management of the HF.

 Goals of treatment: Decrease intravascular volume Decrease venous return Decrease afterload Improve gas exchange and oxygenation Improve cardiac function

Administer Medications (see next set of slides) Cardiac glycosides Diuretics Vasodilators Antilipidemics On going assessments Hemodynamic stability: VS, HR, Rhythm, PA catheter Daily weight Monitor electrolytes

 Prevent

complications of immobility

ROM Antiembolic stockings

Diet

restrictions

Low sodium- to decrease fluid retention and subsequent workload on heart CAD modifiable risks etc

Teaching

 Medications

used for Chronic Heart Failure:

Diuretics Vasodilators Nitrates Inotropes Beta-Adrenergic Blockers Positive Inotropes Angiotension II Receptor Blockers

 Dietary

Modification and Nutrition Therapy is critical to people with HF.

Daily weights Low sodium diet Understanding the S/S of fluid retention

 Nursing

Diagnoses include, but are not limited to

Impaired gas exchange Anxiety Excess fluid volume Activity intolerance

 When

medications are not enoughtreatment options may include:.

Cardioversion Cardiac resynchronization therapy with internal cardioverter-defibrillator Cardiac transplantation