heart failure nur240 lecture 4 1r. kolk, revised 11/09 j. borrero

HEART FAILURE

NUR240

Lecture 4

1R. Kolk, revised 11/09 J. Borrero

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Heart Failure

• Also called pump failure

• Left-sided heart failure

• Right-sided heart failure

• High-output failure

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Etiology

• Heart failure is caused by systemic hypertension in 75% of cases.

• About one third of clients experiencing myocardial infarction also develop heart failure.

• Structural heart changes, such as valvular dysfunction, cause pressure or volume overload on the heart.

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Etiology

• A syndrome of Pulmonary and/ or Systemic congestion due to C.O

• Heart is unable to pump enough blood to meet tissues O2 requirements

Pulmonary pressure fluid in alveoli (PULMONARY EDEMA)

Systemic pressure fluid in tissues(PERIPHERAL EDEMA)

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ETIOLOGY & RISK FACTORS

Cardiac pathology that changes heart’s performance

____________________________________________________________________________________

Risk Factors:

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Compensatory Mechanisms

• Sympathetic nervous system stimulation

• Renin-angiotensin system activation

• Myocardial hypertrophy

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LOCATION

Heart failure classified according to location of ventricular failure

One ventricle may fail independently of another, but failure in one will impact on the other.

L sided failure- pulmonary congestion

R sided failure- peripheral congestion

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Left-Sided Heart Failure

• Manifestations include:– Weakness– Fatigue– Dizziness– Confusion– Pulmonary congestion– Shortness of breath– Oliguria– Organ failure, especially renal failure– Death

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(L) SIDED HF

Tissue hypoxia occurs because heart is unable to efficiently pump blood

CLINICAL SIGNS of pulmonary congestion:Dyspnea OrthopneaCough WT. gainFatigue Anxiety/ restless

S3 CracklesCardiomegaly HR BP

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Right-Sided Heart Failure

• Manifestations include:– Distended neck veins, increased

abdominal girth– Hepatomegaly (liver engorgement)– Hepatojugular reflux– Ascites– Dependent edema– Weight: the most reliable indicator of fluid

gain or loss

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(R) SIDED HF

Blood “BACKS UP” into venous circulation. High oncotic pressure pushes fluids into tissues.

CLINICAL SIGNS:

CVP SUDDEN WT. GAIN

JVD DEPENDENT EDEMA

FATIGUE LIVER CONGESTION

LETHARGY ASCITES

ORTHOPNEA ANOREXIA

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Assessments

• Laboratory assessment- electrolytes,

• BNP- B type natriuretic peptide.

Normal =0

• Radiographic assessment

• Electrocardiography

• Echocardiography, TEE

• Pulmonary artery catheters

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Nursing Assessments

• O2 Saturation• Vital Signs• Heart Rhythm• Lung Sounds• Level of dyspnea• Serum Electrolytes

• Daily weights• Changes in LOC• I & O• Coping ability of pt

and family• Signs of drug toxicity

JCAHO Core Measures for HFEvery patient 100% of the time!

HF-1: Written discharge instructions

HF2: An evaluation of LVS function (Ejection fraction)

HF3: ACE or ARB for LVS function

HF4: Adult smoking cessation advice/counseling

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GOAL

Nursing Dx?

Enhance O2 supply

Work of heart by promoting contractility

Interventions:

1. Adequate ventilation

2. Maintain cardiac function

3. Promote rest

4. Other

5. Medication

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Nursing Interventions

1. ADEQUATE VENTILATION

• Monitor respirations, breath sounds

• Administer O2

• Position- high-Fowlers

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Interventions

2. MAINTAIN CARDIAC FUNCTION• Monitor heart sounds

• Pulmonary Artery Catheter Measurements

CVPPulmonary Artery PressurePulmonary Capillary Wedge

PressureCardiac Output

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Interventions

3. Promote rest until patient is stable

strain on heart

BR promotes cardiac efficiency

Elevate legs to enhance venous return

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Interventions

4. MISC.• Monitor LOC

• Assess edema

• Provide adequate nutrition

• Provide emotional support• Maintain diet restrictions as

prescribed (Na and fluid)

MEDICATION

5. Medication

• Improve myocardial muscle function

• Restore C.O. & SV

• Reduce cardiac demands

Natrecor (nesiritide)- Human B-type natriuretic peptide

causes natriuresis in acute HF

loss of Na and vasodilation

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MEDICATIONS

Fluid load, Preload, Afterload

• Improve contractility

Workload of the heart

ACE inhibitors & Diuretics

Digoxin

Dobutamine

“Blockers”

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Drugs That Enhance Contractility

• Digitalis– Digitalis toxicity includes anorexia, fatigue,

muscle weakness,changes in mental status.– Monitor heart rate for 1 full minute.Hold for <60– Monitor electrolytes– Take same time each day

• Other inotropic drugs including dobutamine, dopamine

• Beta-adrenergic blockers

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Improve contractility Inotropic agents

Digoxin: cardiac glycoside force of myocardial contraction &

slows HR( C.O. venous pressure, diuresis)

• Narrow therapeutic range:– Monitor for toxicity– Digitalization:

dobutamine, dopamine, milrinone (Primacor)

Advanced Calculations for IV Meds ordered/Kg/Minute

1. Convert to like units, such as mg to mcg or lb to kg

2. Calculate desired dosage per minute: mg/kg/min X kg = mg/min3. Calculate the dosage flow rate in mL/min Dosage on hand = Dosage desired/minAmt solution on hand X amt desired/ min4. Calculate the flow rate in mL/hour mL/min X 60 min/h = mL/hr

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Homework

1.Dobutamine 250mg / 250 mL D5W to infuse at 5 mcg/kg/min.

Weight- 80 kg

Flow rate on pump-

2.Dopamine 800 mg/ 500 mL D5W to infuse at 4 mcg/kg/min.

Weight- 190 lbs.

Flow rate on pump-27

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Afterload Reducing Agents

• ACE inhibitors-enalapril (Vasotec)

captopril (Capoten)

• Beta-blockers- carvedilol (Coreg)

• metoprolol (Lopressor XL)

• Angiotensin receptor II blockers

losartan (Cozaar)

• Nitrates- preload and afterload

•

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DIURETIC THERAPY

Increases excretion of Na+/H2O/K

Sites of action differ

Result in varying degrees of ‘lyte imbalance

Categories: Loop, Thiazide, K+-sparing

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NURSING INTERVENTIONS

DIURETIC THERAPY- give early in day

• Monitor WT.

• Assess for edema

• Strict I&O

• Monitor electrolytes

• Nutrition = Low Na+ diet,

K + supplements

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LOOP DIURETICSMORE POTENT ACTION

furosemide (LASIX)

bumetamide (BUMEX) PO/ IVACTION: at loop of Henle, K+ loss, Na+/Cl- excretionADVERSE EFFECTS: orthostatic hypotension, may digitalis toxicity, hypokalemia

Teach: K rich foods, po K, S&S hypokalemia

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THIAZIDE DIURETICS

Useful for maintenance

• HCTZ (Hydrochlorothiazide)

Action: excretion of Na+/Cl- & H2O

Adverse effects: orthostatic hypotension, may digitalis toxicity

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K+ Sparing Diuretics

Maintenance therapy – conserves K+, has a gradual diuretic effect

Spironolactone (Aldactone)

Action: blocks reabsorption of Na+/Cl-

Adverse effects: Hyperkalemia

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PULMONARY EDEMA

Rapid fluid accumulation in lung spaces that has leaked from engorged pulmonary capillaries

Etiology – most common cause is sudden deterioration of LV function

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Potential for Acute Pulmonary Edema due to Left Sided HF

• Interventions include:– Assess for early signs, such as crackles in

the lung bases, dyspnea at rest, tachycardia, disorientation, and confusion.

– Rapid-acting diuretics are prescribed, such as Lasix or Bumex.

– IV morphine sulfate– Oxygen and/or intubation – Strictly monitor fluid intake and output.

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Clinical signs

LV diastolic pressure pulmonary pressure

• Lungs become “stiff” due to fluid buildup, resulting in hypoxia_____________________________________________________________________________________

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Nursing Interventions

• Administer O2 to relieve hypoxia & dyspnea

• CPAP,PEEP

• Assess breath sounds and monitor respirations

• Pulmonary Artery Catheter

• Hi fowler’s position

• Urinary catheterization

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Aminophylline

Bronchodilator given to relieve wheeze/ bronchospasms that may occur

IVPB loading dose, then IV continuous drip

Monitor closely for adverse effects: GI upset, nervousness, HR, H/A, tremors

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Cardiogenic Shock

• Occurs with extensive LV injury perfusion to vital organs

• Degree of shock, directly relates to level of ventricular failure

• Results in: ______________ ____________________________ ______________

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Cardiogenic Shock

Significant reduction in SV & CO causes drop in pressure & poor tissue perfusion a/r/o LV MI

• Clinical signs:– BP, pulse, peripheral pulses– confusion/ agitation (cerebral hypoxia)– cold/ clammy skin– urine output– Resp distress– Chest pain

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Treatment

• Hemodynamic monitoring

• Reduce demand on the heart

• Improve oxygenation

• Improve tissue perfusion

• Intra-aortic balloon pump

• Inotropic Meds to BP, workload

• Correct underlying pathophysiology

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NCLEX TIME

The nurse is awaiting the arrival of a client from the ER who is being admitted with a LVMI. The nurse should be alert for which S&S of left-sided heart failure?

A. Jugular vein distentionB. HepatomegalyC. DyspneaD. CracklesE. Tachycardia

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NCLEX TIME

Harvey is a 76-year-old man being followed up by his nurse practitioner for congestive heart failure (CHF). Which assessment finding would be typically found in an older adult?

• A.Orthostatic hypotension in conjunction with drug therapy for CHF

• B.Clearing of crackles immediately after medication treatment

• C.Auscultation of crackles• D.Digitalis toxicity

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NCLEX TIME

Carlos is prescribed digoxin after having open heart surgery and postoperative atrial fibrillation. Which statement, if made by the client, demonstrates the need for further teaching regarding his digoxin medication?

• A.“I should notify my doctor if my pulse is less than 60 or more than 100 beats/min.”

• B.“I need to keep my laboratory appointments.”• C.“I should not take my digoxin at the same time

as antacids or laxatives.”• D.“If I forget to take my digoxin one day, I can

double up on the dose the next day

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NCLEX TIME

• Mrs. Clark is an 83-year-old woman admitted with symptoms of heart failure. Her nurse, after performing the assessment, tries to decipher between right- and left-sided heart failure. Which symptoms below are consistent with left-sided heart failure?

• A. Weight gain, jugular distention, and distended abdomen

• B. Fatigue, weakness, and palpitations• C. Agitation, blood tinged, frothy sputum, dyspnea• D. Anorexia and nausea, distended abdomen, and

enlarged liver

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NCLEX TIME

Provide the rationale

for each of the

following therapies:

Therapy Rationale

O2

Diuretics

Bedrest

Inotropic agents

Vasodilators

Fluid restriction

Sodium restriction