Transcript CHF-Valvular-3-of-42

Congestive Heart Failure
&
Valvular Disease
Keith Rischer RN, MA, CEN
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Todays Objectives…
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Review essential cardiac patho concepts
Compare and contrast left-sided heart failure to right
Describe special considerations for older adults with
heart failure
Discuss the prevention of complications for patients
with heart failure
Prioritize nursing care for clients with heart failure
Identify common nursing diagnoses and collaborative
problems for patients with heart failure
Evaluate the effects of interventions for reducing
preload and afterload through pharmacological
management
Compare and contrast common valvular disorders
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Introduction
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Definition of CHF
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Etiology
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Left sided vs. Right sided
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Rt sided
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HTN
MI
COPD
Systolic vs. Diastolic
Ejection Fraction
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50-70% normal
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Cardiac Output
CO
= Stroke volume x heart rate
SV (80cc) x HR (80)= 6400cc (6.4 lpm)
• Daily pumps 1800 gallons
• 657,000 gallons every year
• Over 80 year lifetime:
• 52,560,000 gallons
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Definitions
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Pre-load
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Stroke volume
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primarily venous blood return
to RA
Right and left side of heart
filling pressure
(atria>ventricles)
Pressure/Stretch in ventricles
end diastole
Amount of blood ejected from
the ventricle with each
contraction
Systole
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Contraction; myocardium are
tightening and shortening
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Definitions
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Inotropic
state/contractility
Afterload:
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Force of resistance that
the LV must generate to
open aortic valve
Correlates w/SBP
Diastole
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Muscle fibers lengthen, the
heart dilates, and cavities
fill with blood
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Patho: Starling’s Law of the Heart
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Maximum efficency of CO achieved when
myocardium stretched appx 2 ½ times length
Think rubber band
CO decreased with lower preload/filling
pressures or too high
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Compensatory Mechanisms in CHF
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Increased Sympathetic
Nervous System
Stimulation
Renin-angiotensin system
activation
Natriuretic peptides
 BNP
Ventricular hypertrophy
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Acute Pulmonary Edema:
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Elevated capillary pressure within the lungs
 fluid pushed from circulating blood to
interstitial tissues  then to the alveoli,
bronchioles, and bronchi
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Nursing Assessment:Left Failure
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Dyspnea
Cough
Bilateral crackles
Orthopnea
PND
Pulmonary Edema
S3 (ken-tuck-ee)
confusion
fatigue and muscular weakness
nocturia
increase retention of sodium and water due to lowered
glomerular filtration  edema
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Nursing Assessment: Right Failure
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Dependent edema –
 early sign
 symmetric pitting edema
 Bedrest-sacral edema
 anasarca- late sign of
CHF
Ascites
Anorexia, nausea and
bloating
Cyanosis of nail beds
Anxious, frightened,
depressed
Weight gain >2# daily
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Diagnostic Assessment
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Chest x-ray
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12 lead EKG
Echocardiogram
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Cardiac Enlargement
assess ejection
fraction
Labs
BNP
 Liver enzymes…AST,
ALT
 Creatinine/GFR
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Acute Left Failure/Pulmonary Edema:
Collaborative Management:
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O2 treatment
Drug Treatment
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Diuretics
Vasodilators-NTG
MS
Digitalis
Semi- Fowler’s position
Frequent Heart and Lung Assessment
Dietary Restrictions
Planned rest periods
Weigh daily
Report to MD immediately:
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persisting productive cough; dyspnea; pedal edema;
restlessness
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Drug therapy:
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Diuretics
ACE Inhibitors
Beta Blockers
Calcium Channel Blockers
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Nitroglycerine
Positive Inotropic agents
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Digitalis
Beta Adrenergic Stimulator
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Dopamine,Dobutamine
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Pharmacologic: Diuretics
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Mechanism of Action:
Thiazides, Loop,
Potassium Sparing
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S/E:
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fluid and electrolyte
imbalances
CNS effects
GI effects
Nursing
Considerations:
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Monitor for orthostatic
hypotension
Hypokalemia
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Angiotensin Converting Enzyme
(ACE) Inhibitors
Mechanism of Action
 S/E:
Hypotension
 cough
 Hyperkalemia…esp w/CHF, CKD, DM
 Angioedema
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Facial/laryngeal swelling
Nursing considerations:
Do not use with potassium sparing diuretic
 Metabolized by liver-excreted by kidneys
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Adrenergic Inhibitors:
Beta Blockers
Mechanism of Action
 Recommended for initial drug therapy of
uncomplicated HTN (along with diuretic)
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S/E:
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Orthostatic hypotension
bradycardia
bronchospasm
Nursing considerations:
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monitor pulse regularly
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Calcium Channel Blockers
Amlodipine, Diltiazem, Nifedipine
Mechanism of Action:
S/E:
 Nausea
 H/A
 Peripheral edema
Nursing considerations:
 use with caution in patients with heart failure
 Orthostatic changes
 contraindicated in patients with 2nd or 3rd degree heart block
 Concurrent use w/b-blockers incr risk of CHF
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Vasodilators
Mechanism of Action-NTG
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Vasodilater-predominant on venous system by relaxing smooth muscles of
vessels
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Dilates coronary arteries/improves collateral flow
• Up to 20% normal coronaries…30-40% pre/post stenosis
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Decreases LVEDP…why?
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Decreases O2 needs myocardium
Side effects
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HA, hypotension, tachycardia
Hydralazine
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arterial vasodilator
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Priority Nursing Diagnosis
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Impaired Gas exchange r/t ventilation perfusion
imbalance
Decreased Cardiac Output r/t
altered contractility, preload and afterload
Activity Intolerance r/t imbalance between O2
supply and demand
Knowledge Deficit
Activity schedule
 Recognizing worsening heart failure
 Medications
 Diet therapy
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Valvular Heart Disease:Mitral
Valve
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Mitral Stenosis
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Mitral Regurgitation
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Patho
Patho
Mitral Valve Prolapse
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Patho
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Valvular Heart Disease:Aortic Valve
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Aortic Stenosis
Patho
 Causes
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Congenital
Atheroclerosis
Calcification
Aortic Regurgitation
(Insufficiency)
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Patho
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Treatment Valvular Disease
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Non-surgical
Management
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Diuretics
Beta blockers
Digoxin
Antibiotics
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Before any invasives
Coumadin-if artificial valve
Surgical Management
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Balloon Valvuloplasty
Open heart
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Pericarditis
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Patho
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Assessment findings
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Open heart
AMI
Friction rub
CP w/insp
CP relieves sitting up
Global ST elevation
Complications
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Pericardial effusion
Cardiac tamponade
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pericardiocentesis
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Endocarditis
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Patho
Etiology
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Clinical Manifestations
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New murmur
Heart failure
Embolic
Diagnosis
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Valve replacement
Structural cardiac defects
Invasive procedures
Transesophageal Echo
+ blood cultures
Interventions
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IV abx
Surgical
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