Transcript Heart Failure

By
Robert Reynoso, RN, CEN
Special Thanks to William Dubois, RN, CEN
OBJECTIVES
 The Registered Nurse
(RN) will understand
cardiac anatomy &
physiology
 The RN will be able to
identify Heart Failure
(HF) risk factors and its
pathophysiology
 The RN will understand
current medical and
nursing management
WHY HEART
FAILURE?
Heart Failure is a significant
medical, economic and social
aspect of healthcare often not
given proper consideration and
care
It is also one of the top
conditions causing
readmission.
Centennial Hills is in the
midst of attaining Heart
Failure Center status
PREVALENCE
 According to American Heart Association (AHA in
2006
 Adults 20 years and older
 5.7 Million (3.2 Million Male)
 Heart Failure (HF) incidence approaches 10 per 1,000
people aged 65 and older
INCIDENCE
 From Circulation. 2002;106:3068–3072
 75% of HF cases have antecedent hypertension
 At age 40, lifetime risk of developing HF for both men
and women is one in five
 At age 40, lifetime risk of HF occurring without
antecedent heart attack is 1 in 9 for men and 1 in 6 for
women
 The lifetime risk doubles for people with blood pressure
(BP) greater than 160/90 mm Hg compared to those
with BP less than 140/90 mm Hg.
RISK FACTORS
 Hypertension (HTN) is a very common risk factor for HF that
has contributed to a large proportion of heart failure cases
among the study’s participants (JAMA. 1996;275:1557–1562.)
 Study of the predictors of HF among women with coronary heart
disease found that diabetes was the strongest risk factor
(Circulation. 2004;110:1424–1430.)
 Prevalence of diabetes is increasing among older persons with
HF
 Diabetes is a significant independent risk factor for death in
these individuals
 Researchers found that the odds of having diabetes for those first
diagnosed with HF in 1999 was nearly four times higher than for
those diagnosed 20 years earlier (Am J Med. 2006;119:591-599.)
MORTALITY
 2005 total deaths from HF: 292, 214
 58,933 additionally listed as underlying cause
 Based on the 44-year follow-up of the National Heart Lung
Blood Institute's (NHLBI) Framingham Heart Study and
20-year follow-up of the offspring cohort:
 80% of men and 70% of women under age 65 who have HF
will die within 8 years
 After HF is diagnosed, survival is poorer in men than in
women, but less than 15 percent of women survive more than
8–12 years. The one-year mortality rate is high, with one in
five dying
 In people diagnosed with HF, sudden cardiac death occurs at
six to nine times the rate of the general population
HOSPITAL DISCHARGES & COST
• Hospital discharges for HF rose from 877,000 in 2005 to
1,106,000 in 2006
 Increase of 171%
 What do you think the estimated direct and indirect cost
of HF in the United States was for 2009?
POP QUIZ
According to the AHA &
International Monetary Fund,
the USA spends more on HF
than the Gross Domestic
Product (GDP) of:
ANSWER
 100 countries have GDP’s
less than what the USA
spent on HF in 2009
 The estimated direct and
indirect cost of HF in the
United States for 2009 is
$37.2 BILLION
PHYSICAL INACTIVITY
New Remote
Control Can Be
Operated By
Remote
TOKYO—Television
watching became even
more convenient this
week with Sony's
introduction of a new
remote-controlled
remote control.
SMOKING
HYPERLIPIDEMIA
Report: Meat Now
America's No. 2
Condiment
 CHICAGO—Though once
defined as just a standalone meal, meat has risen
quickly up the ranks to
become the nation's
second most popular
condiment, according to a
study released by the U.S.
Department of
Agriculture.
OVERWEIGHT & OBESITY
So-Called Obese
Pets Held To
Unrealistic Body
Standards
CHICAGO—To the casual
eye, Tippy might appear to
be a regular Labrador. He
loves sunbathing at the
park, watching squirrels,
and getting loads of
attention from passersby.
DIABETES MELLITUS
ISCHEMIC HEART DISEASE
ILLICIT DRUG ABUSE & ETOH
DILATED CARDIOMYOPATHY
CONNECTIVE TISSUE DISEASES
VALVULAR HEART DISEASE
MYOCARDITIS
AMYLOIDOSIS
SLEEP APNEA
PHARMACOLOGICS
LAYERS OF THE HEART
CARDIAC ANATOMY
THE CARDIAC PACEMAKER
STROKE VOLUME (SV)
 Volume of blood pumped from the heart with each
beat.
 Cardiac Output (CO) x 1000 /Heartrate (HR)
 Normal Range: 60-100mL/beat
CARDIAC OUTPUT (CO)
 Volume of blood being pumped by the heart in a
minute
 CO=Stroke Volume (SV) x Heartrate (HR)
 Normal Range: 4-8 L/min
Mean Arterial Pressure (MAP)
 Average arterial pressure during a single cardiac cycle
 SBP + (2 x DBP) / 3
 Normal Range: 70-105 mm/Hg
EJECTION FRACTION
 Fraction of blood pumped out of a ventricle with each
heart beat. Normal: 60-75%.
 Stroke volume varies by size of patient (adult versus
peds.)
 Applies to both the right and left ventricles
 One can speak equally of the left ventricular ejection
fraction (LVEF) and the right ventricular ejection
fraction (RVEF).
 Without a qualifier, the term ejection fraction refers
specifically to that of the left ventricle
FRANK-STARLING LAW OF THE HEART
 States that the greater the volume of blood entering the
heart during diastole (end-diastolic volume), the greater
the volume of blood ejected during systolic contraction
(stroke volume)
 As the heart fills with more blood than usual, the force of
the muscular contractions will increase.
 This is a result of an increase in the load experienced by each
muscle fiber due to the extra blood entering the heart.
 The stretching of the muscle fibers increases the affinity of
troponin C for calcium, causing a greater number of crossbridges to form within the muscle fibers; this increases the
contractile force of the cardiac muscle.
BOILED DOWN
 Basically, preload is
stretch. The amount of
volume being returned to
the right side of the heart
from systemic circulation.
 Afterload is squeeze. The
amount of resistance the
left side of the heart has to
overcome in order to eject
blood.
PRELOAD
 Preload is the initial stretching of the cardiac myocytes
prior to systole. Preload, therefore, is related to the
sarcomere length. Because sarcomere length cannot be
determined in the intact heart, other indices of preload are
used such as ventricular end-diastolic volume or pressure.
 For example, when venous return is increased, the end-
diastolic pressure and volume of the ventricle are increased,
which stretches the sarcomeres (increases their preload).
 Increased preload increases stroke volume, whereas
decreased preload decreases stroke volume by altering
the force of contraction of the cardiac muscle.
PRELOAD
INCREASED BY





Increased central
venous pressure
Reduced heart rate
Valvular
regurgitation
Increased aortic
pressure
Ventricular systolic
failure
DECREASED BY
 Decreased central
venous pressure
 Increased heart rate
 Inflow valvular
stenosis
 Atrial arrhythmias
 Ventricular diastolic
failure
AFTERLOAD
 Afterload can be thought of as the "load" that the heart
must eject blood against. In simple terms, the
afterload is closely related to the aortic pressure.
 Afterload is increased when aortic pressure and
systemic vascular resistance are increased, by aortic
valve stenosis, and by ventricular dilation. When
afterload increases, there is an increase in endsystolic volume and a decrease in stroke volume.
AFTERLOAD
INCREASED BY
 Hypertension
 Vasoconstriction
PATHOPHYSIOLOGY
 HF is caused by any condition which reduces the
efficiency of the heart through damage or overloading.
Over time these increases in workload will produce
changes to the heart itself. Examples of conditions:
 AMI (in which the heart muscle is starved of oxygen and
dies)
 HTN(which increases the force of contraction needed to
pump blood)
 Amyloidosis (in which protein is deposited in the heart
muscle, causing it to stiffen).
PATHOPHYSIOLOGY
 Heart rate increases, stimulated by more sympathetic
activity in order to maintain cardiac output.
 Initially, this helps compensate for heart failure by
maintaining blood pressure and perfusion but places
further strain on the myocardium increasing coronary
perfusion requirements, which can lead to worsening of
ischemic heart disease
PATHOPHYSIOLOGY
 Hypertrophy of the myocardium means the heart
muscle fibers increase in size in an attempt to improve
contractility.
 Increased stiffness
 Decreased ability to relax during diastole
 Enlargement of the ventricles contributes to the
enlargement and spherical shape of the failing heart.
 The increase in ventricular size also causes a reduction
in SV due to mechanical and contractile inefficiency.
PATHOPHYSIOLOGY
 General effect is one of reduced CO and
increased strain on the heart.
 This increases the risk of cardiac arrest
and reduces blood supply to the rest of the
body.
 In chronic HF, the reduced CO causes a
number of changes in the rest of the body.
THE BRAIN AND HF
 When arterial blood pressure falls, baroreceptors in the carotid
sinus and aortic arch are DE-stimulated
 The brain increases sympathetic activity, releasing
catecholamines into the blood stream.
 Catecholamines:
 Bind to alpha-1 receptors resulting in systemic arterial
vasoconstriction
 Restore BP but also increases total peripheral resistance,
increasing the workload of the heart
 Bind to beta-1 receptors in myocardium increasing the heart
rate, making contractions more forceful and attempting to
increase CO
 Ultimately increasing the amount of work the heart has to
perform
THE KIDNEYS AND HF
 Increased sympathetic stimulation also causes the
hypothalamus to secrete vasopressin (ADH), which causes
fluid retention by the kidneys
 This increases the blood volume and blood pressure.
 Reduced perfusion to the kidneys stimulates the release of
renin –which catalyzes the production of the potent
vasopressor angiotensin.
 Angiotensin and its metabolites cause further
vasoconstriction and stimulate increased secretion of
aldosterone from the adrenal glands.
 This promotes salt and fluid retention which increases the
blood volume.
THE HEART AND HF
B-type natriuretic peptide (BNP)
 A 32-amino-acid polypeptide secreted by the
ventricles of the heart in response to excessive
stretching of myocytes in the ventricles
 Decreases systemic vascular resistance
 Decreases central venous pressure
 Increases natriuresis (gets rid of salt)
EDEMA & FLUID
 Increased peripheral resistance and greater blood
volume place further strain on the heart and
accelerates the process of damage to the
myocardium.
 Vasoconstriction and fluid retention produce an
increased hydrostatic pressure in the capillaries
 This shifts the balance of forces in favor of
interstitial fluid formation as the increased
pressure forces additional fluid out of the blood,
into the tissue
RIGHT SIDED FAILURE
 Failure of the right ventricle leads to congestion of systemic
capillaries.
 Leads to excess fluid accumulation (edema & anasarca)
 Usually affects the dependent parts of the body first
 (Foot and ankle swelling in people who are standing up and sacral
edema in people who are predominantly lying down)
 Nocturia (frequent nighttime urination) may occur when
fluid from the legs is returned to the bloodstream while lying
down at night.
 In severe cases, ascites (fluid accumulation in the abdominal
cavity causing swelling) and hepatomegaly (enlargement of
the liver) may develop

Significant liver congestion may result in discomfort or impaired
liver function. Jaundice and coagulopathy may occur.
SIGNS
 Exam can reveal:
 Pitting peripheral
edema
 Ascites
 Hepatomegaly.
 Jugular venous
distention
LEFT SIDED FAILURE
 Failure of the left ventricle causes congestion of the pulmonary
vasculature and predominantly respiratory symptoms
 Dyspnea on exertion
 In severe cases, at rest
 Increasing dyspnea while supine (orthopnea)may occur
 Often measured in the number of pillows required to lie
comfortably
 In severe cases, the patient may resort to sleeping while sitting up
 Paroxysmal nocturnal dyspnea, a sudden nighttime attack of severe
breathlessness, usually several hours after going to sleep
 Easy fatigue and exercise intolerance are also common complaints
 Compromise of left ventricular forward function may result in
symptoms of poor systemic circulation such as dizziness,
confusion and cool extremities at rest
SIGNS & SYMPTOMS
 Common respiratory signs are:
 Tachypnea and increased respiratory effort
 Rales or crackles heard initially in the lung bases, and when
severe, throughout the lung fields suggest the development of
pulmonary edema
 Cyanosis which suggests severe hypoxemia, is a late sign of
extremely severe pulmonary edema.
 Additional signs indicating left ventricular failure include:
 Heart murmurs which may indicate the presence of valvular
heart disease, either as a cause (e.g. aortic stenosis) or as a
result (e.g. mitral regurgitation) of the heart failure.
SYSTOLIC DYSFUNCTION
 Heart failure caused by systolic dysfunction is “Pump Failure”
 Characterized by a decreased ejection fraction (less than 40%)
 Ventricular contraction is lessened and inadequate for creating an
adequate SV (inadequate CO)
 In general, this is caused by dysfunction or destruction of cardiac
myocytes. Myocytes can be damaged by:
 Inflammation (myocarditis)
 Infiltration (amyloidosis)
 Toxins and pharmacological agents (such as ethanol, cocaine, and
amphetamines) cause intracellular damage
 Congenital diseases such as Duchenne muscular dystrophy (molecular
structure of individual myocytes is affected)
 Ischemia causing infarction and scar formation.

After AMI, dead myocytes are replaced by scar tissue affecting the function of the
myocardium. On echocardiogram, this is seen as abnormal or absent wall motion.
SYSTOLIC DYSFUNCTION
 Because the ventricle is inadequately emptied, ventricular
end-diastolic pressure and volumes increase. This is
transmitted to the atrium.
 On the left side of the heart, the increased pressure is
transmitted to the pulmonary vasculature, and the
resultant hydrostatic pressure favors extravasation of fluid
into the lungs, causing pulmonary edema.
 On the right side of the heart, the increased pressure is
transmitted to the systemic venous circulation and
systemic capillary beds, favoring extravasation of fluid into
the tissues of organs and extremities, resulting in bodily
edema.
DIASTOLIC DYSFUNCTION






HF caused by diastolic dysfunction is:
 Inadequate relaxation
 Stiffer ventricular wall
Diastolic dysfunction causes:
 Inadequate filling of the ventricle
 Inadequate SV
 Elevated end-diastolic pressures
 Ultimately, systolic dysfunction (pulmonary edema in left heart failure, edema in right heart
failure)
Diastolic dysfunction can be caused by processes similar to those that cause systolic dysfunction,
particularly causes that affect cardiac remodeling (AMI, Duchenne MD, etc.)
Diastolic dysfunction may be hidden if systolic function is preserved. The patient may be
completely asymptomatic at rest
Diastolic dysfunction patients are sensitive to:
 Increases in heart rate
 Tachycardia (caused by exertion, fever, dehydration and dysrhythmias such as atrial fibrillation
with RVR)
Adequate rate control (usually with a pharmacological agent that slows down AV conduction such as a
beta-blocker) is therefore key to preventing decompensation.
WHY THE FATIGUE?
 As the heart works harder to meet normal
metabolic demands, it’s ability to increase
CO is impaired
 Exercise intolerance
 Loss of cardiac reserve
 The heart cannot work harder during
exercise or stress (psychologic or
physiologic)
HIGH OUTPUT FAILURE
 CO normal or elevated but still inadequate for the patient’s
needs
 Caused by chronic volume overload, chronic activation of
the sympathetic nervous system and increased hormone
concentrations
 Gradually causes ventricular enlargement, remodeling and
HF.
 Seen in pregnancy, thyrotoxicosis, Paget’s Disease, beriberi
(B1), AV fistulas and anemia
FUNCTIONAL CLASSIFICATION
 New York Heart Association Functional Classification
 The classes (I-IV) are:




Class I: no limitation is experienced in any activities; there are
no symptoms from ordinary activities.
Class II: slight, mild limitation of activity; the patient is
comfortable at rest or with mild exertion.
Class III: marked limitation of any activity; the patient is
comfortable only at rest.
Class IV: any physical activity brings on discomfort and
symptoms occur at rest.
STAGES OF HEART FAILURE
 The American College of Cardiology/American Heart
Association working group introduced four stages of
heart failure:
 Stage A: High risk for developing HF in the future but
no functional or structural heart disorder
 Stage B: Structural heart disorder but no symptoms
 Stage C: Previous or current symptoms of HF in the
context of an underlying structural heart problem but
managed with medical treatment
 Stage D: Advanced disease requiring hospital-based
support, a heart transplant or palliative care.
AN INCONVENIENT TRUTH
 Daily weights
 Never use the ER stated
weight
 Weigh patient same time
everyday
 Ideal time is on night shift
(0500-0700)


Before physician rounds
Establish procedure with
AM care set-up
 Input & Output (I & O’s)
 “BRP,” “Foley” and similar
are unacceptable
DIET & LIFESTYLE CHANGE
 Arguably the most difficult aspect to change
 Nursing Considerations





Exercise Tolerance
Digestive Factors
Degree of Knowledge Deficit
Religious & Cultural Factors
Economics
PHARMACOLOGICAL
 ACE Inhibitors
 The “ ‘Prils”
 Block the effects
angiotensin II
 Nursing Considerations




Monitor renal function
May increase potassium
(EKG) and decrease
sodium
Fall risk (may cause
dizziness)
Dry cough
 Lisinopril (ZESTRIL,




PRINIVIL)
Fosinopril (MONOPRIL)
Benazepril (LOTENSIN)
Captopril (CAPOTEN)
Enalapril (VASOTEC)
PHARMACOLOGICAL
 Diuretics
 Furosemide (LASIX),
HCTZ, Torsemide
(DEMEDEX), Bumetanide
(BUMEX)
 Diurese the patient
 Nursing Considerations




Monitor renal function &
electrolytes
Daily weights (metric) at
same time without failure
Fall risk r/t dizziness
I & O’s
PHARMACOLOGICAL
 Beta Blockers
 The “ ‘ols”
 More effective heartbeat.
Lowers heart beat and
blood pressure. Protects
your heart from the
harmful effects of
prolonged epinephrine
and norepinephrine
stimulation seen in HF
 Nursing considerations

Monitor EKG and BP
 Metoprolol (TOPROL,




LOPRESSOR)
Carvedilol (COREG)
Labetolol (TRANDATE,
NORMODYNE)
Atenolol (TENORMIN)
Esmolol (BREVIBLOC)
PHARMACOLOGICAL
 Inotropes
 Dobutamine (DOBUTREX)
 Primary mechanism is direct stimulation of β1 receptors
of the sympathetic nervous system
 Not a good idea in ischemic heart disease because it
increases heart rate and thus increases myocardial
oxygen demand
 Nursing considerations



CVC placement
Monitor for tachydysrrhythmias
I & O’s
PHARMACOLOGICAL
 Aldosterone receptor
antagonists: Spironolactone
(ALDACTONE)
 Affect the urinary balance
of water and salts

Weak diuretic
 Potassium-sparing
 Nursing considerations
 Monitor renal function &
electrolytes
 Monitor EKG r/t electrolytes
 Fall risk
 I & O’s
PHARMACOLOGICAL
 Recombinant neuroendocrine hormones
 Nesiritide (NATRECOR)
 Nesiritide is the recombinant form of human B-type
natriuretic peptide (normally produced by the
ventricular myocardium.)
 Nesiritide works to facilitate cardiovascular fluid
homeostasis through counterregulation of the reninangiotensin-aldosterone system, stimulating cyclic
guanosine monophosphate, leading to smooth muscle
cell relaxation.
 In simpler terms, it promotes vasodilation, natriuresis,
and diuresis
MORE NATRECOR
 Nursing considerations
 Monitor electrolytes, renal function & EKG
 BNP will be abnormal
 Daily weight; I & O’s
 Fall risk
PHARMACOLOGICAL
 Vasopressin receptor antagonists
 “Vaptan” class of drugs contains a number of
compounds with varying selectivity, several of which
are either already in clinical use or in clinical trials as
of 2009
 A new class of medication, the "vaptan" drugs, act by
inhibiting the action of vasopressin on its receptors
which deal with the modulation of blood pressure and
kidney function
DEVICES-PACERS & AICD
 Pacemaker
 Implanted Cardiac Defibrillators (ICD’s)

Cardiac Resynchronization Therapy
(CRT) or Biventricular Pacing
 Helpful if cardiac depolarization &
repolarization do not occur rapidly
and evenly.
 Left ventricle may contract a
fraction of a second after the
right ventricle instead of
simultaneously
 This lack of coordination affects
the ability of your heart to pump
effectively
 A device may produce shorter
and more uniform contraction
thus more effective pumping
DEVICES-INTRA AORTIC BALLOON
PUMP
 Mechanical device used to
increase cardiac output
 Consists of a cylindrical balloon
that sits in the aorta and
counterpulsates
 Bridging device
 Deflates in systole increasing
forward blood flow by
reducing afterload
 Inflates in diastole increasing
blood flow to the coronary
arteries
 The balloon is inflated during
diastole by a ECG or pressure
transducer controlled
mechanism, at the distal tip of
the catheter
VAD
 Ventricular Assist Device (VAD)
 Mechanical circulatory device that is used to partially or completely
replace the function of a failing heart.
 Some VADs are intended for short term use, typically for patients
recovering from AMI or cardiac surgery, while others are intended
for long term use (months to years and in some cases for life),
typically for patients suffering from HF (“bridge to transplantation”)
 Outcomes have improved dramatically in recent VAD patients,
despite an increasingly high-risk patient population. These data
suggest that advances in device technology and medical therapies,
as well as a multidisciplinary approach, have improved survival on
VAD therapy.

FROM European Journal of Cardio-Thoracic Surgery (Elsevier) 34 (2):
281–288. Improved survival in patients with ventricular assist device
therapy: the University of Wisconsin experience".
ULTRAFILTRATION
 Ultrafiltration is removal of excess fluid by a dialysis
device. Composition of fluid is adjusted by the
nephrologist
 Aquapheresis removes excess salt and water using a
different type of device with a lower flow rate
 Not currently available in Southern Nevada
 Nursing consideration
 IV access: Vas-Cath
 Monitoring of vital signs, I & O, daily weight
SURGICAL REMODELING
 The Dor Procedure
 Pioneered in 1985 by Vincent Dor, MD
 He introduced EndoVentricular Circular Patch Plasty
(EVCPP), or the Dor procedure

Method for restoring a dilated left ventricle to its normal, elliptical
geometry.
 The Dor procedure would prove to be the best option of
ventricular remodeling
 EVCPP is a relatively easy procedure that covers all aspects of
successful heart restoration—restores ventricular shape,
increases ejection fraction, decreases the left ventricular end
systolic volume index (LVESVI), and allows for complete
coronary revascularization.
VALVE REPLACEMENT
TRANSPLANTATION
 No cardiac transplant
surgeons in Nevada
 Only kidney (UMC)
 Closest are:
 LA (USC, UCLA,
Cedars-Sinai)
 Salt Lake City
 Phoenix
 Loma Linda
AT DISCHARGE
 Legible and appropriate







instructions
Medication Regimen
Lifestyle & Diet Changes
Potassium-rich foods if
appropriate
Daily weights at same time!
How to take a pulse or
monitor BP
The importance of Primary
Care Follow-Up
When to call PCP, go to
Urgent Care/ER or call 911
EDUCATION
 Science, theories and art are dynamic. What was acceptable
practice even 5 years ago can change!
 Keep your yourself up-to-date with scientific literature
 Challenge yourself with your CE!
 Join a professional organization
 Emergency Nurses Association (ENA)
 American Association of Critical Care Nurses (AACN)
 American Academy of Medical-Surgical Nurses (AAMSN)
 Obtain your board certification
 Certified Emergency Nurse (CEN)
 Critical Care Registered Nurse (CCRN)
 Certified Medical-Surgical Registered Nurse (CMSRN)