Care of Patients with

Cardiac Problems
Lecture II Part 2

Mary L. Dunlap
ALT IV Spring 2016
 Heart Failure

Also called pump failure, general term for
the inability of the heart to work effectively
as a pump leading to insufficient perfusion
of body tissue with vital nutrients &
oxygen
Heart Failure
 Etiology

Heart failure is caused by systemic
hypertension in 75% of cases.
About one third of patients
experiencing myocardial infarction also
develop heart failure.
Structural heart changes, such as
valvular dysfunction, cause pressure or
volume overload on the heart.
 Heart Failure

New York Heart Association Classification
Class I No limitation in physical activity
asymptomatic
Class II Symptoms with strenuous exercise
Class III Symptoms with mild exercise
Class IV Symptoms at rest
 Types of Heart Failure

Left-sided heart failure
Right-sided heart failure
High-output failure
 Left-Sided Heart Failure

Decreased tissue perfusion from poor cardiac
output & pulmonary congestion from ↑pressure
in the pulmonary vessels indicate L ventricular
failure
Formerly known as congestive heart failure
Typical causes—hypertension, coronary artery
disease, valvular disease involving mitral or
aortic valve
 Left-Sided Heart Failure

Two types of left-sided heart failure:
Systolic heart failure
Diastolic heart failure
 Left-Sided Heart Failure

Systolic heart failure (systolic ventricular
dysfunction) results when the heart is unable
to contract forcefully enough during systole to
eject adequate amounts of blood into the
circulation.
Often called “forward failure” due to ↓ CO
and fluid back up into the pulmonary system.
 Left-Sided Heart Failure

Symptoms: related to inadequate tissue
perfusion due to ↓ CO
 Weakness
 Fatigue
 ↓ exercise tolerance
 Left-Sided Heart Failure

Diastolic heart failure results when the L
ventricle is unable to relax adequately during
diastole. This “stiffening” disrupts the
normal filling to ensure adequate CO
Causes: ↓ ventricular compliance due to
hypertrophic & cellular changes and
impaired relaxation of heart muscles
 Left-Sided Heart Failure

Symptoms results from ↑ pressure &
congestion behind the ventricle:
S.O.B.
Tachypnea
Respiratory crackles
Pulmonary congestion
 Right-Sided Heart Failure

Typical causes—left ventricular failure, right
ventricular MI, pulmonary hypertension
Right ventricle not able to empty completely
 Right-Sided Heart Failure

Symptoms result of ↑ volume and
pressure in the venous system and
peripheral edema:
Distended neck veins
Liver enlargement
Nausea/anorexia

 Differential Diagnosis of
Heart Failure

Right-sided Failure Left-sided Failure
 Gradual onset  Sudden onset
 Milder symptoms  Sever symptoms
 Systemic edema  Pulmonary edema
 S.O.B.
 Liver congestion
 Nocturnal dyspnea
 Dependent edema
 Orthopnea
 Abdominal distention  Wheezing
 Distended neck veins  Hemoptysis
 S.O.B./cough/Orthopnea  Cyanosis
 High-Output Failure

Cardiac output remains normal or
above normal
Caused by increased metabolic needs
of hyperkinetic conditions such as:
Septicemia
Anemia
Hyperthyroidism
 Acute versus Chronic

Acute HF is the abrupt onset of a
myocardial injury(MI) resulting in
suddenly ↓ cardiac function & signs of ↓
CO
Chronic HF progression deterioration of
the heart muscle due to cardiomyopathies,
valvular disease or CHF
Compensatory Mechanisms

Sympathetic nervous system
stimulation
Renin-angiotensin system (RAS)
activation
Other chemical responses:
B-type natriuretic peptide (BNP)
Myocardial hypertrophy
Compensatory Mechanisms

 Compensatory Mechanisms
 Assessments

History & Physical
Psychosocial assessment
Laboratory assessment
Imaging assessment
Electrocardiography
Pulmonary artery catheters
 History & Physical

Question pt. about history of hypertension,
angina, MI, rheumatic heat disease, valvular
disorders, endocarditis and pericardis
Pt.’s perception of activity tolerance,
breathing pattern, sleeping pattern urinary
pattern
Knowledge of HF
S&S will depend on type of HF
 Psychosocial Assessment

HF is chronic and debilitating
Anxiety & frustration common
Dyspnea ↑anxiety level
Pt. with advanced HF high risk for depression
Assess pt. & family for anxiety & depression
Ask about methods they use to cope
Notify provider
 Laboratory assessment

Serum Electrolyte measured to evaluate
fluid and electrolyte status
UA, BUN, serum creatinine, creatinine
clearance levels, evaluate renal function
Liver function tests and ALT, AST, LDH,
serum bilirubin, total protein & albumin
levels evaluate HF effect on liver function
 Laboratory assessment

TSH &TH levels to evaluate for
hyperthyroidism and hypothyroidism since they
can be a primary or a contributing cause of HF
ANF/ANH and BNP hormones released by the
heart muscle in response to changes in fluid
levels. Elevated in HF
ABG’s evaluate gas exchange in lungs and
tissues
 Diagnostic Assessments

Chest X-ray evaluate for cardiomegaly of the
heart and vascular congestion
Radionuclide studies (thallium imaging) can
indicate the presence and cause of HF
Multigated angiographic scans (MUGA)
provide information about L ventricular ejection
fraction & velocity, typically low in HF pt.
 Diagnostic Assessments

Electrocardiography to identify changes
associated with ventricular enlargement
and to detect dysrhythmias, myocardial
ischemia, or infarction
 Diagnostic Assessments

Echocardiography with Doppler flow studies
(Transthoracic or Transesophageal)will
evaluate L ventricular function
Pulmonary artery catheters allow the
assessment of cardiac function & volume
status in acutely ill patients. Measurements
can confirm the diagnoses & guide the
management of HF
 Interdisciplinary Care

Goal is to slow the progression of HF,
reduce cardiac workload, improve cardiac
function, and control fluid retention.
Treatment is based on the evolution and
progress of the HF.
Nursing Diagnoses


?
 Drug Therapy

Hemodynamic Regulation: interventions to
improve stroke volume including reducing
afterload & preload, and cardiac muscle
contractility.
Variety of classes of drugs to manage HF
Nurses role is to administer drugs, monitor for
their therapeutic & adverse effects, and educate
the pt. and family about these medications
 Drug Therapy To Reduce
afterload

Drugs that reduce afterload: by relaxing the
arterioles & arterial vasodilators can reduce the
resistance to L ventricular ejection (afterload) &
improve CO.
Angiotensin-converting enzyme (ACE)
inhibitors
Angiotensin-receptor blockers (ARB’S)
Human B-type natriuretic peptides
 ACE inhibitors

Can improve & prolong the quality of life for HF
pt.’s.
1st line therapy for CHF
At risk for hypotension, so start slowly with low
dose
Increase vasodilation by blocking conversion of
angiotensin I to angiotensin II; reduce workload of
failing ventricle by reducing blood return and
decreasing vasoresistance.
 ACE inhibitors

They are recommended for both
symptomatic and asymptomatic HF pt.’s
with ejection fraction (EF) of 40% or lower
Contraindicated in pt.’s with heart block
and bilateral renal artery stenosis
 ARB’s

Block aldosterone and inhibit sodium and
water retention, decreasing fluid overload
Recommended for pt.’s with either
symptomatic or asymptomatic HF, EF of 40%
or lower, and ACE inhibitor intolerance
Candesartan(Atacand), Irbesartan (Avapro),
Losartan(Cozaar), Valsartan (Diovan)
 Human B-type natriuretic
peptides

Nesiritide (Natrecor) improves renal glomerular
filtration, augments diuresis and decreases
afterload.
Give through a separate line since it is
incompatible with most medication
Administer IV bolus over 60 sec followed with
continuous infusion for up to 48⁰
Monitor BP & P because significant ↓in BP may
occur
 Drug Therapy To Reduce
Preload

Preload Reduce Drugs attempt to decrease
volume & pressure in the L ventricle,
optimizing ventricular muscle stretch &
contraction
Preload reduction appropriate for HF
accompanied by congestion with total body
Na & H₂O overload
 Diuretics

Diuretics: enhance renal secretion of Na &
water by reducing volume thus decreasing
preload
Loop diuretics are most effective for treating
fluid volume overload. Inhibit Na, K, & Cl,
reabsorption in kidneys, which increases Na
& water excretion and reduces preload
 Diuretics

Thiazide & thiazide-like diuretics do not
inhibit K reabsorption. Used in pt.’s that do
not respond to loop diuretics
With progression of HF pt. may develop
resistance to diuretics. May need to use 2
types of diuretics (monitor renal function
BUN & creatinine levels)
 Nitrates

Nitrates produce both arterial & venous
vasodilatation, thus deceasing volume &
improving L ventricular function.
 Sodium Nitroprusside

Sodium nitroprusside is a potent vasodilator
used to treat acute HF. Causes excessive
hypotension often given with dopamine or
dobutamine to maintain BP
Monitor BP when starting therapy or ↑
dosage
12⁰ free period to prevent tolerance
 Nutritional Therapy

Goal reducing Na and water retention
Decrease Na intake to 3g daily(no added
salt)
If 2g daily is needed pt. will need to
eliminate high sodium food (e.g. ham,
bacon, pickles) and all salt when cooking
 Contractility Drugs

Contractility Drugs enhance contractility of the
heart.
Positive inotropic(glycoside) drugs are most
commonly used- digoxin (Lanoxin)
Reduces exacerbations of HF & hospitalizations
when added to a regimen of ACE inhibitors or
ARB’s, beta blockers and diuretics
 Contractility Drugs

Watch for dig toxicity: anorexia, fatigue,
changes in mental status,
dysrhythmia(PVC’s)
Monitor apical pulse and do not give if less
than 60bpm
 Contractility Drugs

Beta-adrenergic agonists is another inotropic
drug. Dobutamine
Beta adrenergic blockers reverse effects of
prolonged exposure to increased sympathetic
stimulation.
May prevent cardiac remodeling- Left
ventricular dilatation & hypertrophy
 Nonsurgical Options

Continuous positive airway pressure (CPAP)
improves obstructive sleep apnea. It also
improves CO and EF by ↓ afterload and
preload, BP and dysrhythmias
 Nonsurgical Options

Cardiac resynchronization therapy(CRT) also called
biventricular pacing, uses a permanent pacemaker or
a pacemaker in combination with an implantable
cardioverter/defibrillator. CRT creates more
synchronous ventricular contractions to improve EF,
CO, and mean arterial pressure.
This Tx is indicated for pt.’s with class III or IV HF &
EF of less than 35%
Improves pt.’s ability to perform ADL’s
 Nonsurgical Options

Gene therapy replaces damaged genes
with normal or modified genes through a
series of injections of growth factor into
the L ventricle
Indicated for pt.’s in end stage HF who are
not candidates for transplant surgery.
 Nonsurgical Options

Ventricular assisted device a mechanical
pump implanted to work with the pt.’s
heart.
Short-term use as a bridge to transplant or
long term destination therapy which
increases length and quality of life.
 Plan of Care

Pt.’s who are not prepared for discharge are at
high risk for recurrent admissions for HR
Family support or home health aids can help
with ADLs
Education important for self management table
37-4 p777
Provide oral, written and video instructions
about drug regimen
 Signs of Worsening or
Recurrent HF

Rapid weight gain
↓ in exercise tolerance lasting 2-3 days
Cough lasting more than 3-5 days
Excessive urination at night
Dyspnea or angina at rest
Worsening angina
↑swelling in feet ,ankles or hands
 Surgical Therapy

Cardiac transplant treatment of choice for end
stage heart disease. More than 90% of pt.’s
return to normal, unrestricted functional
abilities
Most common procedure leaves posterior walls
of atria, superior & inferior vena cavae, &
pulmonary veins which are attached to donor’s
heart
 Cardiac Transplant

Nursing care similar to care of any cardiac surgical
pt.
Bleeding most common concern in early
postoperative period.
Chest tube drainage monitored & gently milked to
maintain patency to prevent cardiac tamponade
(compression of the heart)
Pacing wires
Monitor for infection or rejection
 Heart Failure Summary

 Causes Treatment and living well
 Living with CHF/HF
 Pulmonary Edema

Exacerbation of HF
Assess for early S&S: cough, crackles in
bases of lungs, dyspnea at rest,
confusion.
Acute S&S: tachycardia, anxious, moist
cough, productive frothy-blood tinged
sputum, cold clammy, cyanotic skin
 Pulmonary Edema

Document exact level of crackles
Administer O2- 5-6 L/min facemask or 10-15 L/min
by non-rebreather mask with reservoir
Place pt. on pulse ox & cardiac monitor to keep O2
sat’s above 90%
Place pt. in high fowler’s
Possible IV diuretic administration
Urine output within 5-15 min after diuretic
administration
 Valvular Heart Disease

Acquired valvular dysfunction: mitral
stenosis, mitral regurgitation, mitral valve
prolapse, aortic stenosis & aortic
regurgitation
Tricuspid valve affected following
endocarditis in IV drug abusers
 Mitral Stenosis

Usually caused by rheumatic heart disease or
bacterial endocarditis, rarely is congenital
Chronic & progressive
Valve leaflets fuse & become stiff while the
chordae tendineae contract & shorten
Narrowing of the mitral valve obstructs blood
flow from the L atrium into L ventricle during
diastole.
Mitral valve desease
 Mitral Stenosis

Mild usually asymptomatic
As opening narrows & pressure in lungs ↑pt.
c/o dyspnea on exertion, orthopnea,
paroxysmal nocturnal dyspnea, palpitations,
& dry cough
 Mitral Regurgitation

Rheumatic heart disease major cause of mitral
regurgitation & coexists with some degree of
mitral stenosis
Congenital defects also may cause mitral
regurgitation
The fibrotic & calcific changes prevent the
valve from closing completely during systole
 Mitral Regurgitation

Incomplete closure of the valve allows backflow of
blood into L atrium when the L ventricle contracts
during systole
During diastole regurgitant output again flows from
atrium to ventricle along with normal blood flow.
↑volume must be ejected during next systole
Atrium &ventricle dilate & hypertrophy to
compensate
 Mitral Regurgitation

Progress slowly
Symptoms develop when L ventricle fails due to
chronic volume overload: fatigue, chronic
weakness due to reduced CO
Later dyspnea on exertion & orthopnea develop
Progresses to R sided HF, distended neck veins,
liver enlarges, pitting edema
 Mitral Valve Prolapse

Cause often unclear.
Can result from acute or chronic
rheumatic damage, ischemic heart
disease
Commonly affects people with
connective tissue disorder
 Mitral Valve Prolapse

Collagen tissue in the valve leaflets &
elongated chordae tendineae impair closure
of the valve, allowing the leaflets to billow
into L atrium during systole
Some ventricular blood regurgitates into L
atrium
Most pt.’s are asymptomatic
 Mitral Valve Prolapse

Symptoms: chest pain, which is atypical,
palpations, dizziness & syncope
Increased risk for bacterial endocarditis
Thrombi could form on valve leaflets:
embolization could cause TIAs
 Aortic Stenosis

Most common valve dysfunction
May be idiopathic, due to congenital
defect, rheumatic damage or degenerative
changes
Stenosis obstructs blood flow from the L
ventricle into the aorta during systole
 Aortic Stenosis

The opening into the aorta narrows ↑
the work of the L ventricle to eject it’s
volume into the aorta.
Ventricle hypertrophies to maintain an
adequate SV & CO
 Aortic Stenosis

Symptoms result from fixed CO: dyspnea,
angina & syncope on exertion
Late stages marked fatigue, debilitation &
peripheral cyanosis
Surface area of the valve is 1cm or less
surgery in indicated urgent basis
 Aortic Regurgitation

Thickened & contracted valve cusps, scarring,
fibrosis & calcifications impede complete valve
closure
Blood from the aorta flows back into the L
ventricle during diastole
L ventricle compensates by dilating to
accommodate the larger blood volume &
hypertrophies
 Aortic Regurgitation

Symptoms: remain asymptomatic for years
due to the compensatory mechanisms of the
L ventricle
Disease progresses L ventricle failure occurs
major symptoms: dyspnea on exertion,
orthopnea, paroxysmal nocturnal dyspnea,
nocturnal angina with diaphoresis
 Assessment

Patient may become suddenly ill or slowly
develop symptoms over many years.
Question patient about attacks of rheumatic
fever and infective endocarditis and about
possibility of IV drug abuse.
Obtain chest x-ray, echocardiogram, and
exercise tolerance test.
 Common Nursing
Diagnoses

Decreased Cardiac Output related to altered
stroke volume
Impaired Gas Exchange related to ventilation
perfusion imbalance
Activity Intolerance related to inability of the
heart to meet metabolic demands during
activity
Acute Pain related to physiologic injury agent
(hypoxia)
 Nonsurgical Management

Management depends on the valve that is
affected & the degree of impairment
Nonsurgical therapy focuses on drug
therapy & rest
Drug therapy, including diuretics, beta
blockers, digoxin, oxygen are used to
improve the symptoms of HF
 Nitrates in aortic stenosis ↓L ventricle
preload & can cause syncopy
 Nonsurgical Management

Prophylactic antibiotic is required before any
invasive procedures
Maintaining cardiac output with atrial fibrillation if
it develops
Anticoagulant is used for valvular disease with
chronic atrial fibrillation to prevent formation of
thrombi
Rest with limited activity due to the ↓CO inability to
meet the metabolic demands.
 Surgical Management

Reparative procedures have become the
preferred procedure due to problems with
thrombi, endocarditis, & left ventricular
dysfunction after valve replacement
 Surgical Management

Balloon valvuloplasty enlarges the mitral
orifice & improves leaflet mobility with a
balloon catheter from the femoral vein,
through atrial septum, to mitral valve where it
is inflated. Provides immediate relief from
symptoms
Monitor pt. for bleeding post procedure at
cath insertion site
 Surgical Management

Direct, or open, commissurotomy done
during open heart surgery. The valve is
visualized, thrombi removed from atria,
fused leaflets incised and debrides
calcium is removed, along with widening
the orifice
 Surgical Management

Mitral valve annuloplasty is a
reconstructive procedure that makes the
valve ring that attaches to the leaflets
smaller
Replacement procedures with prosthetic or
biologic(tissue) valves
Heart Valves
 Infective Endocarditis

Microbial infection(viruses, bacteria, fungi)
involving the endocardium
Most common infected organism is strep
viridans or aures
Occurs primarily in patients who abuse IV
drugs, have had valve replacements, have
experienced systemic infections, or have
structural cardiac defects
 Infective Endocarditis

Possible ports of entry—oral cavity, skin
rash, lesion, abscess, infections, surgery, or
invasive procedures including IV line
placement
 Infective Endocarditis

Early detection is imperative due to the
high mortality rate
 Many pt.’s are missed diagnosed
Recurrent fever from 99⁰-103⁰
 HF most common complication
 Manifestations

Murmur
Heart failure
Arterial embolization
Splenic infarction
Neurologic changes
Petechiae (pinpoint red spots)
Splinter hemorrhages
chart 37-9 p784
 Diagnostic Assessment

Blood culture
Echocardiography
The most reliable criteria for
diagnosing endocarditis include
positive blood cultures, a new
regurgitant murmur, and evidence of
endocardial involvement by
echocardiography
 Interventions

Antimicrobials main treatment, appropriate
drug in sufficiently high dose, IV route for 4-6
weeks, usually penicillin's or cephalosporin's
Anticoagulants are of no value in preventing
embolization from vegetations.
Patient’s activities are balanced with
adequate rest.
 Surgical Management

Removing the infected valve
Repairing or removing congenital shunts
Repairing injured valves and chordae
tendineae
Draining abscesses in the heart or
elsewhere
 Community Based Care

PT. and family able to administer medications at
home
Care for the infusion site
Followed by home health nurse
Good hygiene, including oral
Pt.’s will need to inform all providers about their
endocarditis to receive prophylactic antibiotics
Notify provider of signs of return of disease
 Pericarditis

Inflammation or alteration of the
pericardium, the membranous sac that
encloses the heart
 Pericarditis

Acute viral commonly follows a respiratory
infection
Dressler’s syndrome occurs 1-2 wks. After an
MI
Post-pericardiotomy syndrome occurs after
cardiac surgery
 Pericarditis

Chronic constrictive pericarditis occurs due
to chronic inflammation that causes a fibrous
thickening of pericardium caused by: TB,
radiation therapy, renal failure, or metastatic
cancer.
 Assessment

Substernal precordial pain radiating to left
side of the neck, shoulder, or back
Grating, oppressive pain, aggravated by
breathing, coughing, swallowing
Pain worsened by the supine position;
relieved when the patient sits up and leans
forward
Pericardial friction rub
 Interventions

Pain management: NSAIDs
Corticosteroids if no pain relief in 48-96 hrs. and it
is not bacterial pericarditis
Bacterial(acute): antibiotics & pericardial drainage
Chronic due to malignant disease: radiation or
chemotherapy
Chronic constrictive: Pericardiectomy, surgical
excision of pericardium
 Cardiac Tamponade

Pericardial effusion is a complication that
can develop. It occurs when the space
between the parietal & visceral layers fill
with fluid.
Cardiac tamponade develops when the
fluid is in excess & restricts diastolic
ventricular filling → CO↓
 Cardiac Tamponade

Acute Cardiac tamponade can occur
with volumes as small as 20-50 mL
accumulate rapidly
If the fluid accumulates slowly, the
pericardium can stretch to accommodate
several hundred mL
 Cardiac Tamponade

Pericardiocentesis- fluid is removed to relieve the
pressure on the heart
Under echocardiographic or fluoroscopic &
hemodynamic monitoring, cardiologist inserts
8in 16-18g pericardial needle into the pericardial
space. The ST & T wave are monitored for
changes. Catheter is inserted through needle and
fluid is removed. Drain may be temporarily place
 Rheumatic Carditis

Sensitivity response that develops after an
upper respiratory tract infection with group
A beta-hemolytic streptococci
 How the infection causes inflammatory
lesions in the heart in not established
Inflammation is noted in all layers of the
heart
 Rheumatic Carditis

Inflammation results in impaired contractile
function of the myocardium, thickening of
the pericardium, and valvular damage
Formation of Aschoff bodies, small nodules
in the myocardium that are replaced by scar
tissue
 Clinical Manifestations

Tachycardia
Cardiomegaly
New or changed murmur
Pericardial friction rub
Precordial pain
Changes in electrocardiogram
Indications of heart failure
Existing streptococcal infection
 Cardiomyopathy

Subacute or chronic disease of cardiac muscle
Classified into four categories based on
abnormalities in structure & function:
1. Dilated cardiomyopathy
2. Hypertrophic cardiomyopathy
3. Restrictive cardiomyopathy
4. Arrhythmogenic right ventricular
cardiomyopathy
 Interventions

Drug therapy: diuretics, vasodilation
agents, cardiac glycosides to ↑CO
Implantable cardiac defibrillators and
antidysrhytmic's to control life threating
dysrhythmias
Toxin exposure avoidance
Alcohol avoidance
 Surgical Management

Ventriculomyomectomy: ventricular septal
myectomy excises a portion of the
hypertrophied ventricular septum to create a
wider outflow tract
Percutaneous alcohol septal ablation widens L
ventricular outflow tract
Heart transplantation treatment of choice for
pt.’s with Dilated cardiomyopathy(DCM)
 Heart Transplant

Criteria for candidate selection:
Life expectance less than 1 yr.
Younger than 65
NYHA class III or IV
Normal or slightly ↑pulmonary vascular resistance
Absence of active infection
Stable psychosocial status
No evidence of current drug or alcohol abuse