Heart Failure - Student

8/3/2019 Heart Failure - Student

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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

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Heart Failure - Student