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NU 331
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Syndrome of pulmonary or systemic circulatory
congestion caused by decreased myocardial
contractility, resulting in inadequate CO to meet
oxygen requirements of the tissues.
Incidence of CHF increases with aging
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Primary causes are disorders producing decreased
myocardial contractility:
CAD
Valvular heart disease
HTN
Cardiomyopathy
Dysrhythmias
Cor pulmonale secondary to lung disease
Pericarditis
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Heart Failures hallmarks arevasoconstriction 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 agingof America, and survival rates after cardiacevents.
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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
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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 andelevated pressure in the systemic veins &
capillaries.
Biventricular: inability of both ventricles to
pump blood effectively.
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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
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As cardiac output fall the body will attemptto compensate (continued) RAAS: Renin-Angiotension-Aldosterone System-
as blood flow to the kidney decreases, the kidney
releases renin (through juxtaslumerularapparatus stimulation) which converts toangiotension to angiotension II which causes theadrenal cortex to release aldosterone, causingsodium and water retention, increasing
peripheral vasoconstriction and BP
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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
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As the body attempts to compensateall
these things together, the SNS, RAAS, ADH-
all cause increased cardiac workload and
myocardial dysfunction resulting in abnormalshaped contractile cells and increased
ventricular mass.
Impaired contractility = less effective
pumping
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Two symptoms commonly seen in the heartwith 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 massof the wall of the myocardium in response to the
workload
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Heart failure usually manifests itself as
biventricular failure- although usually one
side decompensates and fails first.
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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
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Fatigue
Dyspnea, orthopnea,and/or paroxysmal
nocturnal dyspnea Tachycardia
Edema- peripheral,hepatomegaly, ascites
3 lb weight gain in 2days is potentially
problematic
Nocturia
Skin changes
Dusky coloring
Cool, damp
Shiny, swollen lowerextremities without hair
Behavioral changes
Restlessness, memoryissues
Angina pain
Weight changes Poor diet
Renal failure
Hepatomegaly
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Congestion occurs primarily in the lungs from
back up of blood into the pulmonary veins and
capillaries because of left ventricular pumpfailure.
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)
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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
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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 leftsided CHF
Elevated central venous pressure in right sided CHF
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Congestion in systemic circulation from right
ventricular pump failure
Blood backs up in systemic circulation (rightatrium and venous circulation), causing
increased hydrostatic pressure and produces
peripheral and dependent pitting edema.
Usually see venous congestion in kidneys, liverand GI tract as well
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Assessment Findings:
Dependent pitting edema
Anasarca
Weight Gain
Nausea and vomiting
Jugular Vein Distention
Liver congestion (hepatomegaly), ascites, or weakness
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Potential Complication of Heart Failure:
Dysrythmias
Most common is atrial fibrillation
Normal depolarization is disrupted with the
enlargement of the heart
Hepatomegaly
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 cirrhosisdevelops
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Identify the cause of heart failure, thefactors that are aggravating the symptoms,and the current status of the individual tomake a plan of care that meets their
individual needs. Every case is a little different, most people
with HF have other comorbid conditions thathave to additionally be considered in
management of the HF.
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Goals of treatment: Decrease intravascular volume
Decrease venous return
Decrease afterload
Improve gas exchange and oxygenation
Improve cardiac function
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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
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Medications used for Chronic Heart Failure:
Diuretics
Vasodilators
Nitrates Inotropes
Beta-Adrenergic Blockers
Positive Inotropes
Angiotension II Receptor Blockers
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Dietary Modification and Nutrition Therapy is
critical to people with HF.
Daily weights
Low sodium diet Understanding the S/S of fluid retention
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Nursing Diagnoses include, but are not
limited to
Impaired gas exchange
Anxiety Excess fluid volume
Activity intolerance
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When medications are not
enoughtreatment options may include:.
Cardioversion Cardiac resynchronization therapy with internal
cardioverter-defibrillator
Cardiac transplantation