heart failure lecture students

7/31/2019 Heart Failure Lecture Students

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CARDIAC HEMODYNAMICS

Basic function of the heart: to pump blood

Measured by CO: HR x SV

SV: amount of blood pumped out of the

ventricle with each contraction

HR: primarily controlled by the ANS

Determinants of SV PRELOAD

AFTERLOAD CONTRACTILITY

Precise measurement of these factors requires

hemodynamic monitoring


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PRELOAD

Is the amount of blood presented to the ventricle

just before systole

Increases pressure in the ventricle --->

stretching the ventricular wall (by blood to

produce optimal recoil & forceful ejection of

blood) ---> too little or too much muscle fiber

stretch decreases the volume of blood ejected


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PRELOAD

Major Determinants of PRELOAD

Venous return of blood to the heart creating

the volume of the blood entering the ventricle

during diastole

Ventricular compliance: the elasticity or

amount of give when blood enters the

ventricle Decrease elasticity due to thickening of the

muscles (hypertrophic cardiomyopathy)

Increased fibrotic tissue within the ventricle (MI)


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AFTERLOAD The amount of resistance to the ejection of blood from

the ventricle

To eject blood: the ventricle must overcome the

resistance caused by tension in the aorta and systemic

vessels

Inversely related to SV

An increase in afterload causes the ventricle to work

harder and may decrease the amount of blood ejected

DETERMINANTS

The diameter and distensibility of the great vessels

(aorta / PA)

Competence of the semilunar valves

Significant vasoconstriction, HTN, or a narrowed

valvular opening from stenosis ----> resistance

(afterload) increases


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CONTRACTILITY

The force of contraction is related to the

status of the myocardium

Increase contractility and SV Catecholamines released by sympathetic

stimulation during exercise

Administration of positive inotropic

medications

MI: necrosis and fibrosis of the myocardial

cells


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NONINVASIVE ASSESSMENT OF

CARDIAC HEMODYNAMICS RV PRELOAD:

estimated by measuring the jugular venous

distention (JVD) LV AFTERLOAD:

Mean Arterial Blood Pressure

OVERALL CARDIAC FUNCTIONING: Activity Tolerance


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INVASIVE ASSESSMENT OF

CARDIAC HEMODYNAMICS CENTRAL VENOUS CATHETERS

PULMONARY ARTERY CATHETER

Intacardiac pressures

PAP

CO


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Heart Failure The inability of the heart to pump sufficient blood

to meet the needs of the tissues for oxygen andnutrients

A syndrome characterized by fluid overload orinadequate tissue perfusion

The term HF indicates myocardial disease, in

which there is a problem with the contraction of

the heart (systolic failure) or filling of the heart

(diastolic failure). Some cases are reversible.

Most HF is a progressive, lifelong disorder

managed with lifestyle changes and

medications.


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ETIOLOGY

Coronary artery disease

Cardiomyopathy

Hypertension Valvular disorders

Primary cause of HF

atherosclerosis of the coronary arteries (60%)


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CLINICAL MANIFESTATIONS

GENERAL

Fatigue

Decreased activity tolerance

Dependent edema

Weight gain CARDIOVASCULAR

Third heart sound (S3)

Apical impulse enlarged with left lateraldisplacement

Pallor and cyanosis

Jugular venous distention (JVD)


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RESPIRATORY

Dyspnea on exertion

Pulmonary crackles that do not clear with cough

Orthopnea

Paroxysmal nocturnal dyspnea (PND)

Cough on exertion or when supine


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CEREBROVASCULAR

Unexplained confusion or altered mental status

Lightheadedness

RENAL

Oliguria and decreased frequency during the day

Nocturial

GASTROINTESTINAL

Anorexia and nausea Enlarged liver

Ascites

Hepatojugular reflux


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Clinical Manifestations

Right-sided failure RV cannot eject sufficient amounts of blood, and

blood backs up in the venous system. This resuts

in peripheral edema, hepatomegaly, ascites,

anorexia, nausea, weakness, and weight gain.

Left-sided failure

LV cannot pump blood effectively to the systemic

circulation. Pulmonary venous pressuresincrease, resulting in pulmonary congestion with

dyspnea, cough, crackles, and impaired oxygen

exchange.

Chronic HF is frequently biventricular.


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LEFT-SIDED HEART FAILURE

Dyspnea

Cough

Pulmonary crackles

Low oxygen saturation levels

S3 or ventricular gallop

Orthopnea PND

Nocturia


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RIGHT-SIDED HEART FAILURE

JVD

Edema Hepatomegaly

Ascites

Anorexia and nausea


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Classification of Heart Failure

NYHA classification of HF

Classification I, II, III, IV

ACC/AHA classification of HF

Stages A, B, C, D

Treatment guidelines are in place for each

stage.


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NYHA CLASSIFICATION OF

HEART FAILURECLASS SIGNS & SYMPTOMS PROGNOSIS

I Ordinary physical activity does not cause undue

fatigue, dyspnea, palpitations, or chest pain

No pulmonary congestion or peripheral

hypotension

Patient is considered asymptomatic

Usually no limitations of ADLs

GOOD

II Slight limitation on ADLs

Patient reports no symptoms at rest but

increased physical activity will cause symptoms

Basilar crackles and S3 murmur may be

detected

GOOD


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NYHA CLASSIFICATION OF

HEART FAILURECLASSIFICATION SIGNS & SYMPTOMS PROGNOSIS

III Marked limitation on ADL

Patient feels comfortable atrest but less than ordinary

activity will cause symptoms

FAIR

IV Symptoms of cardiac

insufficiency at rest

POOR


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ACC / AHA CLASSIFICATIONOF HF

CLASSIFICATION CRITERIA

STAGE A Patients at high risk for developing left ventricular

dysfunction but without structural heart disease or

symptoms of heart failure

STAGE B Patients with left ventricular dysfunction or structural

heart disease who have not developed symptoms of

heart failure

STAGE C Patients with left ventricular dysfunction or structuralheart disease with current or prior symptoms of heart

failure

STAGE D Patients with refractory end-stage heart failure

requiring specialized interventions


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ASSESSMENT & DIAGNOSTIC

FINDINGS Echocardiogram

CXR

ECG

Serum Electrolytes

BUN

Creatinine


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ASSESSMENT & DIAGNOSTIC

FINDINGS

TSH

CBC BNP

Urinalysis

Cardiac Stress Testing or Cardiac Catheterization


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Medical Management of HF

Eliminate or reduce etiologic or contributoryfactors.

Reduce the workload of the heart by reducing

afterload and preload. Optimize pharmacologic and other

therapeutic regimens.

Prevent exacerbations of HF. Medications are routinely prescribed for HF.

Promote a lifestyle conducive to cardiac

health


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PHARMACOLOGIC THERAPY

Angiotensin-converting enzyme inhibitors Angiotensin II receptor blockers

Hydralazine and Isosorbide Dinitrate

Beta-blockers Diuretics

Digitalis

Calcium Channel Blockers Intravenous Infusions

Other medications


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ACE INHIBITOR

Slow the progression of HF

Improve exercise tolerance Decrease the number of hospitalizations for HF

Form: oral, IV


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ACE INHIBITOR Promote vasodilation and diuresis by decreasing afterload

and preload -----> decrease the workload of the heart

Vasodilation reduces resistance to left ventricular ejection

of blood -----> diminish the hearts workload and improving

ventricular emptying

Promoting diuresis: decrease the secretion of aldosterone

(hormone causing kidneys to retain sodium & water)

Stimulate the kidneys to excrete Na & H20 (retaining K)

-----> reducing left ventricular filling pressure & decreasing

pulmonary congestion


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ACE INHIBITOR

THERAPEUTIC EFFECTS Dec BP and afterload

Relieve signs and symptoms of HF

Prevents progression of HF KEY NURSING CONSIDERATION

Hypotension

Hypovolemia

Hyperkalemia

Hyponatremia

Alterations in Renal Function


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ACE INHIBITOR Lisinopril (Prinivil, Zestril)

Benazepril (Lotensin)

Captopril (Capoten)

Enalapril/Enalaprilat (Vasotec)

Fosinopril (Monopril)

Moexipril (Univasc)

Perindopril (Aceon)

Quinapril (Accupril)

Ramipril (Altace)

Trandolapril (Mavik)


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ANGIOTENSIN II RECEPTORBLOCKERS

ARBs have similar hemodynamic effects with

ACEI

Dec BP and afterload

Dec SVR

Improved CO

Relieves signs and symptoms of HF

Prevents progression of HF

KEY NURSING CONSIDERATION

Similar with ACEI


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HYDRALAZINE & ISOSORBIDEDINITRATE

Alternative therapy for patients who cant take

ACEI

Nitrates:

Venous dilation -----> reduces the amount of

blood return to the heart -----> lowers PRELOAD

Hydralazine:

Lowers SVR and left ventricular AFTERLOAD

Combination recommended in HF Guidelines


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BETA-ADRENERGIC BLOCKINGAGENTS

BETA BLOCKERS Dilates blood vessels and dec afterload

Dec signs and symptoms of HF

Improves exercise capacity


Dizziness

Fatigue

Hypotension

Bradycardia


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BETA BLOCKERS

Metoprolol (Lopressor, Toprol)

Atenolol (Tenormin)

Carvedilol (Coreg)


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DIURETICS To remove excess extracellular fluid

-----> increasing the rate of urine produced

Dec fluid volume overload

Dec signs and symptoms of HF

KEY NURSING CONSIDERATIONS

Electrolyte abnormalities

Renal dysfunction

Diuretic resistance Dec BP

Monitor I&O

Daily weight


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DIURETICS

LOOP

Furosemide (Lasix)

THIAZIDE

Metolazone (Zaroxolyn)

Hydrochlorothiazide (HCTZ)

ALDOSTERONE ANTAGONIST

Spironolactone (Aldactone)


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DIGITALIS

Increases the force of myocardial contraction

Slows conduction through the AV node

Improves contractility, increasing LV output ---> enhances diuretics

KEY CONCERN: DIGITALIS TOXICITY

DIGOXIN (Lanoxin)

DIGOXIN USE TOXICITY IN


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DIGOXIN USE & TOXICITY INHF

Therapeutic Level: 0.5 2.0 mg/mL

Preparations:

Tablets: 0.125, 0.25, 0.5 mg (Lanoxin)

Capsules: 0.05, 0.1, 0.2 mg (Lanoxicaps)

Elixir: 0.05 mg/mL (Lanoxin Pediatric Elixir)

Injection: 0.25 mg/mL, 0.1 mg/mL (Lanoxin)


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DIGOXIN TOXICITY

Early

Anorexia Nausea & vomiting

Fatigue

Depression Malaise

Changes in HR or rhythm; onset of irregular

rhythm

ECG changes indicating ventricular

dysrhythmias, atrial tachycardia with block,

junctional tachycardia, ventricular tachycardia


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REVERSAL OF TOXICITY

Holding the medication

Monitor serum digoxin level

Severe toxicity: DIGOXIN IMMUNE FAB

(Digibind)


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NURSING CONSIDERATIONS &ACTIONS FOR DIGITALISTHERAPY Assess the patients clinical response to

therapy through evaluation of relief of

symptoms

Dyspnea

Orthopnea

Crackles Hepatomegaly

Peripheral edema


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MONITOR THE PATIENT FOR FACTORS

THAT INCREASE THE RISK OF TOXICITY Hypokalemia

Use of medications that may enhance the effects of

digoxin

Impaired renal function

Before administration

STANDARD PRACTICE: ASSESS FOR APICAL

HR!!!

Monitor for GI side effects

Monitor for Neurologic side effects


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CALCIUM CHANNEL BLOCKERS Vasodilation

Reduction of SVR


Hypotension

Drowsiness or dizziness


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CALCIUM CHANNEL BLOCKERS

Dihydropyridines

Amlodipine (Norvasc) Felodipine (Plendil)

First Gen Ca Channel

Verapamil (Calan0

Nifedipine (Procardia)

Diltiazem (Cardizem)


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INTRAVENOUS INFUSIONS

NESIRITIDE (Natrecor)

32 amino acid recombinant technology BNP

Binds to vascular smooth muscle and endothelial

cells ---> dilation of arteries and veins

Suppression of neurohormones responsible for

fluid retention ---> diuresis

END RESULT preload and afterload unloader

inc SV


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MILRINONE (Primacor) A phosphodiesterase inhibitor delaying the

release of Calcium from intracellular reservoirs

---> prevents uptake of extracellular Calcium by

the cells ---> vasodilation ---> decreasedPRELOAD & AFTERLOAD ---> REDUCED

CARDIAC WORKLOAD

KEY CONSIDERATION

Hypotension

GI dysfunction

Increased ventricular dysrhythmias


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DOBUTAMINE (Dobutrex)

Stimulates the beta-1-adrenergic receptors --->

increase cardiac contractility

KEY CONSIDERATION

Increases the heart rate

Precipitate ectopic beats

Tachydysrhythmias


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OTHER MEDICATIONS FOR HF Anticoagulants

Statins


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Nutritional Therapy

Additional Therapy

Supplemental Oxygen

Other Interventions

CAD: coronary artery revascularization

DYSRHYTHMIAS: ICD

No Improvement with Standard Therapy: CRT

Severe Fluid Overload: ULTRAFILTRATION

End Stage HF: CARDIAC TRANSPLANTATION


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GERONTOLOGICCONSIDERATIONS Age-related changes increasing frequency of

HF

Inc SBP

Inc ventricular wall thickness Inc myocardial fibrosis

Elderly may present with atypical signs &

symptoms

Fatigue

Weakness

Somnolence


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GERONTOLOGIC

CONSIDERATIONS Decreased Renal Function

Resistant to diuretics

More sensitive to changes in volume

Diuretics in elderly men

Requires nursing surveillance for bladder

distention

Nursing Process: The Care of the


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Nursing Process: The Care of thePatient with HF: Assessment Health history

Signs and Symptoms of HF Sleep and activity

Knowledge and coping

Physical exam

Mental status

JVD

Hepatojugular Reflux

Lung sounds: crackles and wheezes Heart sounds: S3 Fluid status/signs of fluid overload

Daily weight and I&O

Assess responses to medications


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Nursing Process: The Care of thePatient with HF: Diagnosis

Activity intolerance and fatigue

Excess fluid volume

Anxiety

Powerlessness

Ineffective therapeutic regimen

(Noncompliance)


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Collaborative Problems/Potential

Complications Hypotension, Poor Perfusion, Cardiogenicshock

Dysrhythmias

Thromboembolism

Pericardial effusion and cardiac tamponade


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Promoting Activity Tolerance Bed rest for acute exacerbations

Encourage regular physical activity; 30-45 minutesdaily

Exercise training

Pacing of activities

Wait 2 hours after eating before doing physical

activity.

Avoid activities in extremely hot, cold, or humid

weather. Modify activities to conserve energy.

Positioning; elevation of HOB to facilitate breathing

and rest, support of arms


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Managing Fluid Volume

Assessment for symptoms of fluid overload

Daily weight

I&O

Diuretic therapy; timing of meds

Fluid intake; fluid restriction

Maintenance of sodium restriction

See Chart 30-4


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Controlling Anxiety

With difficulty maintaining adequate oxygenation Restless and anxious

Overwhelmed by breathlessness

Interfere with sleep

Emotional Stress ---> stimulates SNS

Oxygen administration during an acute event

Promote physical comfort

Provide psychological support

Identify factors contributing to anxiety

How to use relaxation techniques to control anxious

feelings


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Minimizing Powerlessness

Assess factors contributing to a sense of

powerlessness

Lack of knowledge

Lack of opportunities to make decisions

Taking time to listen actively to patients

Provide the patient with decision-making

opportunities Provide encouragement


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Monitoring and Managing Potential

Complications Excessive and repeated diuresis

Hypokalemia

Hyperkalemia

Hyponatremia

Dehydration and hypotension

Increased serum creatinine and

hyperuricemia

P ti t T hi


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Patient Teaching Medications

Diet: low-sodium diet and fluid restriction Monitoring for signs of excess fluid,

hypotension, and symptoms of disease

exacerbation, including daily weight Exercise and activity program

Stress management

Prevention of infection Know how and when to contact health care

provider

Include family in teaching


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CONTINUING CARE

Home health care

HF clinic

Telehealth management

END-OF-LIFE CONSIDERATIONS


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EVALUATION

EXPECTED PATIENT OUTCOMES

Demonstrates tolerance for increased activity

Describes adaptive methods for usual activities

Schedules activities to conserve energy and reducefatigue and dyspnea

Maintains HR, BP, RR, and pulse oximetry within the

targeted range

Maintains Fluid Balance Exhibits decreased peripheral and sacral edema

Demonstrates methods for preventing edema


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EVALUATION


Is less anxious

Avoids situations that produce stress

Sleeps comfortably at night

Reports decreased stress and anxiety

Denies symptoms of depression

Makes sound decisions regarding care and

treatment

Demonstrates ability to influence outcomes


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EVALUATION


Adheres to self-care regimen

Performs and records daily weights

Ensures dietary intake includes no more than 2 to 3 gof sodium per day

Takes medications as prescribed

Reports any unusual symptoms or side effects

Thromboembolism


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Thromboembolism

Decreased mobility and decreased circulation

increase the risk for thromboembolism in

patients with cardiac disorders, including

those with HF.

Pulmonary embolism: blood clot from the legsmoves to obstruct the pulmonary vessels

The most common thromboembolic problem with

HF Prevention

Treatment

Anticoagulant therapy


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Pulmonary Emboli


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Umbrella Filter

P i di l Eff i d C di


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Pericardial Effusion and CardiacTamponade Pericardial effusion is the accumulation of

fluid in the pericardial sac.

Cardiac tamponade is the restriction of heartfunction due to this fluid, resulting indecreased venous return and decreased CO.

Clinical manifestations: ill-defined chest painor fullness, pulsus parodoxus, engorged neckveins, labile or low BP, shortness of breath

Cardinal signs of cardiac tamponade: fallingsystolic BP, narrowing pulse pressure, risingvenous pressure, distant heart sounds


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Assessing for Cardiac Tamponade


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Medical Management Pericardiocentesis

Pericardiotomy


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END

GOODLUCK!!!

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