HEART FAILURE
 atrial fibrillation or tachycardia. Altered
 A clinical syndrome resulting from
structural or functional cardiac disorders that
impairs the ability of the ventricles to fill or
eject blood. It is a clinical syndrome
characterized by signs and symptoms of
fluid overload and inadequate tissue
perfusion. Fluid overload and decreased
tissue perfusion results when the heart
cannot generate CO sufficient to meet the
body demands for oxygen and nutrients
 HF indicates myocardial disease in which
impaired contraction of the heart (systolic
dysfunction) and filling of the heart
(Diastolic dysfunction) may cause
pulmonary or systemic congestion.
 the heart is too weak to pump efficiently so
it can’t provide proper cardiac output to
maintain the body’s metabolic needs.
 Results on the body: organs and tissues will
suffer from the decreased blood flow,
pressure in the heart increases which over
works the ventricles, body can become
congested with fluids (enter into congestive
heart failure) that can cause life-threatening
complications.
 Note: the left ventricle is the largest of all
four chambers which allows for maximum
pumping power. The ability of the ventricle
to empty lessens, the stroke volume falls and
the residual volume increases
Causes of Heart Failure
Mainly due to the heart muscle (specifically the
ventricles) becoming damaged or too stiff.
Remember the mnemonic: Failure
Faulty heart valves
 Valves ensures that blood flows in one
direction. With valvular dysfunction it
becomes difficult for blood to move
forward, increasing pressure within the heart
and increasing cardiac work load leading to
HF.
 AV and SL valve problems (due to
congenital issues or infection (endocarditis)
that causes blood to back flow
(regurgitation) or stenosis (narrowing of the
valves that increases pressure of blood flow
through the valves). This causes the heart to
work harder and become weak over time
resulting to ventricular overload leading HF
Arrhythmias
electrical stimulation impairs myocardial
contraction and decreases the overall
efficiency of myocardial function
Infarction (myocardial)/MI
 Cause by coronary artery disease: part of the
heart muscle dies due to a blockage in the
coronary arteries…muscle become ischemic
and can die because it deprives heart
muscles of oxygen and causes cellular
damage. (main cause of left ventricular
systolic dysfunction). MI compromises
myocardial function by reducing
contractility and producing abnormal wall
motion. The extent of infarction correlates
with Heart failure.
Lineage (congenital)…family history
Uncontrolled Hypertension
 overtime this can lead to stiffening of the
heart walls because with untreated HTN the
heart has to work harder and this causes the
ventricles to become stiff.
 Systemic or Pulmonary HTN- Increases
afterload (resistance to ejection) which
increases cardiac workload and leads to
hypertrophy of the myocardial muscle fibers
that increases contractility. Sustain
hypertension leads to changes that impairs
the heart’s ability to fill during diastole and
the hypertrophied may dilate and fail
(Grossman andPorth, 2014)
Recreational Drug Use (cocaine) or alcohol abuse
Envaders (instead of Invaders): viruses or infections
that attack the heart muscle
Cardiomyopathies
 Various types of cardiomyopathy lead to
heart failure and dysrhythmias.
 Dilated Cardiomyopathy the most common
type of cardiomyopathy causes diffuse
myocyte necrosis and fibrosis leads to HF.
DCM is unknown cause or results from
inflammatory process such as myocarditis or
from a cytotoxic agent such as alcohol
 Hypertrophic cardiomyopathy leads to
severe ventricular hypertrophy and poor
diastolic filling. The myocyte
enlargement, myocyte disarray and
increased amounts of myocardial
fibrosis
Ventricular overload
 Increased preload due to mitral and aortic
regurgitation, atrial or ventricular septal
defects, or rapid volume of IV fluids
 Increased afterload due to aortic or
pulmonary valve stenosis, hypertension and
pulmonary hypertension
Heart failure can be acute or chronic and can be
triggered/exacerbated with:
 High salt intake or fluid (watch fluids)
 Infection
 Uncontrolled atrial fibrillation
 Renal failure
Classification of HF (NY Heart Associatio)
Classificatio Ss and sx
n
1 No limitation of physical activity.
Ordinary activity does not cause
fatigue, palpitation or dyspnea
2 Slight limitation of activity
Comfortable at rest but ordinary
physical activity causes fatigue,
palpitation and dyspnea
3 Marked limitation of physical
activity
Comfortable at rest but less than
ordinary activity causes fatigue,
palpitation and dyspnea
4 Unable to carry out any physical
activity without discomfort
Symptoms of cardiac insufficiency
at rest
If any physical activity is done,
discomfort is increases
TYPES OF HEART FAILURES
Left & Right Side Heart Failure (can have both at the
same time as well)
Left-Sided Heart failure- Most common type of
heart failure
Pathophysiology
 the left side of the heart cannot pump blood
out of the heart efficiently so blood starts to
back-up in the lungs resulting to Pulmonary
Congestion. This occurs when the left
ventricle cannot effectively pump blood out
of the ventricle into the aorta and systemic
circulation.
 The increased left ventricular end-diastolic
blood volume increases the left ventricular
end diastolic pressure, which decreases
blood flow from the left atrium into the left
ventricle during diastole. The blood volume
and pressure build up in the LEFT atrium.
This results to increased Pulmonary blood
volume and pressure in the LUNGS, forcing
the fluids into the PULMONARY TISSUES
and ALVEOLI resulting to PULMONARY
EDEMA and IMPAIRED GAS
EXCHANGE.
 In addition, as the LV decreases its ejection
of blood, it leads INADEQUATE TISSUE
PERFUSION
 Inability of the heart to maintain CO
(Forward Heart Failure).
 Left-sided heart failure is likely to lead to
right-sided heart failure.
 Left-sided heart failure will present with
PULMONARY Signs and Symptoms.
 The left ventricle becomes too weak and
doesn’t squeeze blood out properly….the
heart failure can be either SYSTOLIC OR
DIASTOLIC.
Systolic Heart failure
 “Left ventricular systolic dysfunction”
 Characterized by weak hear muscle
 Systolic is the contraction or “squeezing”
phase of the heart.  
 In systolic dysfunction, there is an issue with
the left ventricle is not able to eject blood
properly out of the ventricle and the organs
can’t get all that rich-oxygenated blood it
just received from the lungs.
 Patients will have a low ejection fraction.
 An EF of 40% or less is a diagnosis for
heart failure.
What is Ejection Fraction?
 Is calculated by subtracting the amount of
blood present in the left ventricle at the end
of the systole from the amount present at the
end of diastole and calculating the
percentage of blood that is ejected.
 A normal EF is 50% (55%-65%) or
greater meaning that more than half of the
 blood that fills inside the ventricles is being
pumped out.
 Ejection fraction is a calculation used to
determine the severity of heart failure on the
left side
 An EF can be measured with an
echocardiogram, heart cath, nuclear stress
test.
Diastolic: “Left ventricular diastolic dysfunction”
 remember diastole is the filling or resting
phase of the heart.
 In diastolic dysfunction, the ventricle is too
stiff and non compliant heart muscle
making it difficult for the ventricle to fill
with blood.
 Since there isn’t an issue with
contraction but filling, the ejection fraction
is NORMAL
Right-Sided Heart Failure:  
 the right side of the heart cannot pump or
eject the “used” blood it received from the
body efficiently so it can’t get the blood
back to the lungs to get replenished with
oxygen.  The causes the blood to back up
peripherally (legs, hands, feet, abdomen).
 Right-sided heart failure causes congestion
of blood in the heart and this increases the
pressure in the inferior vena cava (which
normally brings “used” blood back to the
heart for re-oxygenation). This built-up
pressure causes the hepatic veins to become
very congested with blood which leads to
hepatomegaly and swelling peripherally.
 This occurs when the right side of the heart
cannot eject blood effectively and cannot
accommodate all the blood that normally
returns from the venous circulation.
(Brunner and Suddart,2017)
 RSHF is usually caused from left-sided
heart failure because of the increased fluid
pressure backing up from the left side to the
right. This causes the right side of the heart
to become overworked.
 Other causes: pulmonary heart disease “cor
pulmonale” as a complication from
pulmonary hypertension or COPD.
 Right-sided heart failure presents with
PERPHIERAL SIGNS AND
SYMPTOMS.
Know the difference between the signs and
symptoms of left vs. right sided heart failure.
LEFT-SIDED HEART FAILURE
 will present with PULMONARY
manifestations)
 Remember the
mnemonic DROWNING (these patients are
literally drowning in their own fluid from
the heart’s failure to pump efficiently). The
ss and sx are due to Pulmonary Edema, and
activation RAAS
 Difficulty breathing/Dyspnea- precipitated
by minimal to moderate activity, but also
occurs at rest
 Rales/ Crackles- do not clear with
coughing and detected in early LVHF. O2
sat is also decreases.
 Orthopnea (cannot tolerate lying down…
must sit-up to breath, especially while
sleeping). May use pillows to prop
themselves up in bed or may Sit in a chair,
sleep sitting
Weakness (extremely tired and fatigued due
to shortness of breath and heart can’t
compensate for increased activity.
 Nocturnal Paroxysmal dyspnea- awaking
during sleep with extreme dyspnea because
the LV cannot eject the increased circulating
blood volume that results to increased
pressure in the pulmonary circulation and
shifting of fluids into the ALVEOLI that
impairs gas exchange (CO2 and O2)
 Increased heart rate -due to fluid overload
and the heart is trying to get the blood to
organs but it can’t because of muscle failure.
And this is related to DECREASE SV that
cause the SNS to increase the HR and
complaints of PALPITATION
 Nagging cough (can be frothy or blood-
tinged sputum from fluid overload in the
lungs…very bad sign)
 Gaining weight due to fluid retention-2 to 3
lb in a day or 5 lbs in a week
 Other ss and sx:
 Fatigue, weakness- due to decrease CO, the
body cannot respond to increased energy
demand and has decreased activity tolerance
 Oliguria- due to reduce CO to the kidneys.
 Nocturia- When the patient is sleeping,
cardiac workload is decrease, improving
renal perfusion leading to frequent urination
at night.
 Altered digestion due to decreased GI
perfusion
 Dizziness, confusion, light headedness,
restlessness and anxiety due to decreased
brain perfusion
  Pale and cool clammy skin- due to SNS
stimulation causes the blood vessels to
constrict
 Hypokalemia, clubbing of fingers, S3 and
S4 heart sounds,
 Elevated PAP and PCWP
Right-Sided Heart Failure
 presents with PERPHIERAL SIGNS AND
SYMPTOMS.
 Remember: Mnemonic: SWELLING (fluid
is backing up in the right side of the heart
which causes fluid to back-up in the hepatic
veins and peripheral veins).
 RSCHF will results from COR Pulmonale
due to high blood pressures in the arteries of
the lungs and
 Swelling of legs, hands, liver, abdomen
 Weight gain
 Edema (pitting) due to fluid retention, seen
on the feet and ankles and worsens when the
patient stands or sit for a long time. Edema
may decrease when the patient elevate the
legs
 Large neck veins (jugular venous
distention)- due to fluid retention
 Lethargic (weak and very tired)
 Irregular heart rate (atrial fibrillation)
 Nocturia (frequent urination at night) lying
down elevates the legs and allows the extra
fluid to enter into the vascular system which
allows the kidneys to eliminate the extra
fluid.
 Girth of abdomen increased-signs of
ASCITES (from swelling of the liver and
building up fluid in the abdomen. Sacral
edema is common when patient is on bed
rest because this area is dependent. can’t
breathe well and this causes nausea and
anorexia
 Hepatomegaly- tenderness in the RUQ of
the abdomen results of venous engorgement
of the liver. As hepatic dysfunction
progresses, increased pressure within the
portal vessels may force fluids into the
abdominal cavity causing ASCITES.
Hepatomegaly may increase pressure of the
diaphragm resulting to RESPIRATORY
DISTRESS.
 Anorexia, nausea, and abdominal pain-
results from venous engorgement and
venous stasis
 Elevated CV readings
Tests used to Diagnose Heart Failure:
 Echocardiogram- to determine EF, to
identify anatomic abnormalities, valve
malfunction and confirm the diagnosis
 Chest x-ray and ECG- to assist in diagnosis
 Heart catheterization and Cardiac stress test-
to determine whether CAD and ischemia are
the cause of HF.
 BNP (b-type natriuretic peptide) blood test:
a biomarker released by the ventricles when
there is excessive pressure in the heart due
to heart failure.<100 pg/mL no failure, 100-
300 pg/mL present, 300 pg/mL mild, 600
pg/mL moderate, 900 pg/mL severe
 Pulmonary Arterial Pressure (PAP):
measures pressure in right ventricle or
cardiac status: increased
 Pulmonary Capillary Wedge Pressure
(PCWP): measures end systolic and
dyastolic pressure: increased
 Central Venous Pressure (CVP): indicates
fluid or hydration status
Assessment
 Focuses on the signs and symptoms of HF
 Dyspnea, fatigue, edema, sleep disturbances
due to SOB,
 Asked about how many pillows needed for
sleep, edema
 VS: BP, HR (note for S3) RR, auscultate
lungs to detect crackles or rales and
wheezing, oxygen saturation, LOC changes
due to Low CO and oxygen in the brain,
 JVD-patient is in sitting at 45degree angle,
distention greater than 4 cm above the
sternal angle is an indication of RVHF
 Peripheral pulses- 0 to +3
 Abdomen- look for tenderness and
hepatomegaly
 I and O
 Weigh daily- same time, clothes, scale. 2-3
lbs increase in a day or 5 lbs in a week is
significant change in weight that should be
relay to PHC
Diagnosis
 Decrease CO
 Fluid Volume excess related to disease
process
 Activity intolerance rl to decreased CO and
perfusion
 Anxiety related to ss and sx of HF
Planning and Goals
 To maintain CO oxygen and pumping ability
of the heart.
  To relieve fluid overload
 Reduce fatigue
 To increase ADL as tolerance
 To decrease or manage anxiety
Nursing Interventions for Heart Failure
Role: Assessing, monitoring, intervening, and
educating
Assess patient for worsening symptoms (right-sided
failure…peripheral swelling vs left-sided failure…
pulmonary edema)
Maintain Oxygenation
 O2 per nasal cannula or mask at2-6 L/min as
ordered
 Maintain semi fowlers or high fowlers to
maximize oxygenation by greater lung
expansion.
 Monitor ABG analysis results
To Increased CO
- Administer medications (Digoxin) as
ordered
Reduce Fluid Overload
 Fluid status (may be ordered a Foley
catheter, if on diuretics)
 Cardiac diet (low in salt and fats)
 Fluid restriction (no more than 2 L per day)
 Keep legs elevated and patient in high
Fowler’s to help with breathing and to
reduce pulmonary venous
congestion and ease dyspnea.
 Monitor weight
 Maintain accurate I&O
 Assess for peripheral edema
 Measure abdominal girth daily
 Monitor electrolyte levels
 Lab values: watching BNP, kidney function
BUN & creatinine, troponins levels,
electrolytes (especially potassium…if on
Lasix: waste potassium and low potassium
increases risk of digoxin toxicity)
 Safety (at risk for falls due to fluid status
changes, swelling in legs and feet, and
orthostatic hypotension)
Promoting rest and activity/Reduce Fatigue
 Bed rest or limited activity during acute
phase- it will worsen ss and sx
 Provide overhead table close to the patient to
allow resting of the head and arms
 Gradual ambulation is encourage to prevent
risk of venous thrombosis and embolism due
to immobility
 Activities: Dangling, sitting up in a chair
then walking in increase distances under
supervision because prolong inactivity may
cause pressure ulcer
To reduce anxiety
- Provide psychological comfort and physical
comfort
- Relaxation techniques to control anxious
feelings
- Oxygen may be given to diminished the
work of breathing
- Avoid anxiety provoking situations
Promoting Nutrition
- Control sodium intake
- Bland low calories, ow residue diet during
acute phase
- Frequent small feedings
Promoting elimination
- Avoid straining at defecation which triggers
Valsalva maneuver.VM increases the
cardiac workload
- Encourage use of bedside commode. Lesser
cardiac workload than a bed pan. Using bed
pan involve lifting the hips which triggers
VM
- Administer laxative as ordered ex: Colace
If acute Pulmonary Edema occurs with CHF
- High fowlers with legs slightly lowered to
facilitate breathing and to reduce pre load
- O2 therapy via face mask or nasal cannula
(40-70%(
- Morphine sulfate as ordered. To reduce
preload (venous dilatation) and afterload
(arterial dilatation) and to reduce anxiety
- Administer aminophylline IV as ordered. To
relieve bronchospasm
- Administer digitralis, diuretics. Vasodilators
Administering medications:
Know the drug categories a patient will be taking
with heart failure and what drugs are included in that
category, the pharmacodynamics, and side effects:
To remember the groups of drugs use this mnemonic:
Always Administer Drugs Before A Ventricle Dies!
Ace Inhibitors (angiotensin-converting-enzyme
inhibitors)
 first line of treatment for heart failure with
beta blockers
 end in “pril” Lisinopril, Ramipril, Enalapril,
Captopril
 works by allowing more blood to get to the
heart muscle which allows it to work easier.
 Also, blocks the conversion of Angiotensin I
or Angiotensin II (this causes vasodilation,
lowers blood pressure, allows kidneys to
secrete sodium because it decreases
aldosterone.
 Side effects: dry, nagging cough and can
increase potassium (inhibiting angiotensin II
which decreases aldosterone in the body
which causes the body to retain more
potassium and excrete sodium)
 Monitor K levels it cause hyperkalemia. And
BP it cause Hypotension
ARBs (Angiotensin II receptor blockers):
 end in “sartan” like Losartan, Valsartan
 used in place of ACE inhibitors if patient
can’t tolerate them
 blocks angiotensin II receptors which causes
vasodilation. This lowers blood pressure and
helps the kidneys to excrete sodium and
water (due to the affects that blocking
angiotensin II has on the kidneys…decreases
aldosterone).
 side effects: increases potassium
levels….NO dry nagging cough
Diuretics
 used along with ACE inhibitors or ARBs
 to decrease water and sodium retention
which will decrease edema in the body and
lungs. This allows the heart to pump easier.
 It removed excess extracellular fluid by
increasing the rate of urine with signs of
fluid overload.
 Patients will urinate a lot!
 Loop diuretics (most common) like Lasix or
Furosemide (watch potassium level because
they will waste potassium)
 Thiazides-chlorothiazides, and hydro chloro-
thiazides
 Potassium-sparing diuretics like
“Aldactone” (can cause hyperkalemia,
especially if taking with ACE or ARBs). It
blocks the effects of aldosterone in the distal
tubule/ Aldosterone antagonist
 Diuretics are BEST given early in the
morning or early afternoon to prevent sleep
pattern disturbances related to nocturia
 Give K supplement or K rich foods (Loop
diuretics and Thiazides) as these
medications increase K excretion
Beta Blockers:
 blocks norepinephrine and epinephrine
effects on the heart muscle/it blocks the
adverse effects of SNS
 given in stable heart failure with ACE
inhibitors
 end in “lol” like Metoprolol, Carvedilol and
Bisoprolol
 not for acute heart failure because the
negative inotropic effect on the heart. The
negative inotropic effect causes decrease
myocardial contractility (slows heart) and
decreases cardiac work load.
 It relax blood vessels, lower BP, decrease
afterload, and cardiac workload. Improve
oxygen supply and demand, Promotes blood
flow to the heart, Anti-dysthymic effects
 used in stable heart failure in people
with ventricular systolic dysfunction (there
is a contraction problem with the left
ventricle) and to treat diastolic heart
failure (remember there is a problem with
the heart filling in diastolic dysfunction). It
will help the heart rest so the stiff ventricle
can fill properly and the volume of blood
pumped out increases.
 monitor for bradycardia, masking signs and
symptoms of hypoglycemia in diabetics,
breathing problems in asthmatics and COPD
 Educate patient not to take beta blockers
with grapefruit juice because it slows the
absorption of beta blockers
 side effects: check pulse (bradycardia),
hypotension
 Monitor HR and BP
 No grape juice; mask hypoglycemic signs in
diabetics, respiratory issues in asthmatics
and patients with COPD because beta
blockers can cause bronchiole constriction,
it may worst the condition.
Anticoagulants:
 not used in all patients with heart failure
 Typically, used in patients with heart failure
who are in a-fib because they are at risk for
blood clot formation or certain scenarios of
 left ventricular systolic heart failure when
there is a low ejection fraction of <35%.
Vasodilators:
 Combination of Hydralazine (arterial
dilator) prescribed with a nitrate like Isordil
(venous dilator)- reduces the amount of
blood return to the heart and lowers preload.
 sometimes used in place of an ACE or ARB,
if patient can’t tolerate them
 this causes vasodilation in the arteries and
veins to help decrease the amount of blood
and fluid going back which helps decrease
the work load on the heart
 side effects: low blood pressure, orthostatic
hypotension
 Monitor BP
Digoxin:
 Digoxin (Lanoxin), Crytodigin (Digitoxin),
Lanatoside C (Cedilanid C), Deslanoside
(Cedilanid D)
 Positive inotropic effect that increases the
heart’s ability to contract stronger and it has
a negative chronotropic action that causes
the heart to beat slower
 So, the heart slows down and contracts
stronger which allows the heart to pump
more blood.
 treatment for patients with left ventricular
systolic dysfunction (however, not usually
the first line of treatment due to side effects
and toxicity risks)…used alongside
ACE/beta blockers, and diuretics
 check apical pulse before giving….>60
bpm. If the heart rate is 60bpm and below
120 bpm and above. WITHOLD the drug.
Bradycardia and rebound tachycardia may
occur.
 toxicity issues: monitor patient potassium
level (hypokalemia <3.5 mEq/L) because
hypokalemia increases digoxin toxicity
 S & S of toxicity: nausea, anorexia,
vomiting, visual changes yellowish green,
halos, confusion and bradycardia
 Normal Digoxin range 0.5 to 2 ng/mL
 Evaluate the effectiveness: increased CO,
urine output, strong pulse,
 Antidote for Digitalis Toxicity: Digoxin
Immune Fab (Digibind)
Intravenous Infusions
IV inotropes
- Milrinone (Primacor), Dobutamine
(Dubutrex)
- Increase the force of myocardial contraction
with acute HF
Milrinone (Primacor),
- It increase intracellular calcium within
myocardial cells to increase contractility
- Promotes vasodilation resulting in decrease
preload and afterload and reduce cardiac
workload.
- IV administration
- Monitor BP prior to administer, if there is
hypovolemic, the BP could drop quickly
- SE: Hypotension and ventricular
dysrhythmias. BP and ECG are monitored
closely during and following infusion.
Dobutamine (Dubutrex)
- Given to patient with left ventricular
dysfunction and hypoperfusion
- It increased cardiac contractility and renal
perfusion to enhance urine output
- It also increases the HR and can cause
tachydysrhythmias
Amiodarone (Cordarone)
- Antiarryhtmic drugs in patient with
dysrhythmias particularly ventricular
tachycardia
Nutritional Therapy
LOW SODIUM
 No more than 2 g/day and fluid restriction
(no more than 2 L per day
 Na restriction reduces fluid retention and to
decrease the amount of circulating blood
volume which decreases myocardial work
OXYGEN THERAPY
- To reduce tissue hypoxia
- provided in high concentration by mask or
cannula.
- Consider intubation if:
o O2 saturation cannot be kept >90%
on 100% O2
o PaO2 cannot be kept >60 or on 100
% O2
o Patient displays signs of worsening
cerebral hypoxia
o PaCO2 progressively increases
o Patient becoming exhausted
Surgical management

Percutaneous Transluminal Coronary Angioplasty

- A balloon tip catheter is placed in a coronary
vessel narrowed by plaque
- The balloon is inflated and deflated to
stretch the vessel and flatten the lesion
- Blood flows freely through the unclogged
vessel to the heart.
- To improve the blood flow within the
coronary artery by compressing the
atheroma
Coronary Artery Bypass Graft
 A graft is surgically attached to the aorta and
the other end of the graft is attached to a
distal portion of a coronary vessel.
 Bypasses obstructive lesion in the vessel and
returns to adequate blood flow to the heart
muscle supplied by the artery.
CARDIAC RESYNCHRONIZATION THERAPY
- Involves the use of biventricular pacemaker
to treat electrical conduction defects
- The used of pacing device with leads place
in the RA RV and LV can synchronize the
contractions of of RV and LV
- Improves CO optimizes myocardial energy
consumption, reduces mitral regurgitation
and slows ventricular remodeling process.
Educating:

 Early signs and symptoms heart failure

exacerbation: Shortness of breath, Weight
gain, Orthopnea
 Low salt (allowed 2-3 G sodium per day)
and fluid restriction (no more than 2 L per
day)
 Vaccination to prevent illness, such as
annual flu and to be up-to-date with
pneumonia vaccine
 Exercise aerobic (as tolerated)
 Daily weights (watch for no more than 2-3
lb per day and 5 lbs per week)
 Compliance with medications
 Smoking cessation
 Limiting alcohol
 Patient responsiveness to medication
treatment:
 watch heart rate (Digoxin), respiratory
status, blood pressure (vasodilators cause
hypotension), diuretics (strict intake and
output, daily weights, monitor electrolyte
levels, especially K+)