Transcript Heart failure 2015

Heart Failure
Learning Objectives
 Students will be able to:
 Discuss epidemiology of heart failure in NZ
• Define heart failure – acute and chronic
 Compare the pathophysiology of systolic and diastolic
ventricular heart failure.
 Describe compensatory mechanisms associated with heart
failure
 Describe Left and Right ventricular failure and link to clinical
manifestation of Heart Failure
 Describe nursing interventions and multidisciplinary
management of heart failure including pharmacological
therapy.
New Zealand Epidemiology
• Major public health problem. > 1.3% of population
• Admission rates increased by 10.6% over last 5 years (National
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Heart Foundation of New Zealand)
Average of about 850 deaths per year =2%
Mortality = 20% at 6months and 30% at 12 months
Approximately 8 times higher among Maori males aged 45-65
Hospital admissions about 5,500 per year with a mean duration of
stay 5-16 days (Maori 8-9 times higher)
Accounts for 1.5 -2% of health budget (>$NZ60m)
Occurs on average 10 -15 yrs earlier amongst Maori than nonMaori
Definition of Heart Failure
 Heart failure (HF) is caused by any structural
or functional cardiac abnormality that impairs
the ability of the left ventricle to fill with or
eject sufficient blood to meet the metabolic
needs of the body.
 HF is not a specific anatomic abnormality but
a clinical syndrome characterized by specific
symptoms
http://merck.praxis.md/bpm/bpm.asp?page=BPM01CA06&section=report&ss=1&hilight=cong
estive+heart+failure
Pathology
Cycle of Heart Failure:
Not enough blood is
pumped out of the
ventricles causing the
body to stimulate the
heart to work harder.
The failing heart muscle
is unable to respond and
the pathology of heart
failure becomes worse.
Pathology of Heart Failure
• Classified as systolic or diastolic failure
• Systolic – inability to pump or eject blood - EF
• Diastolic – inability of ventricles to relax and fill
resulting in decreased stroke volume and cardiac
output – EF
• Mixed systolic and diastolic – EF
• Ejection fraction (EF) –blood ejected from left
ventricle with each contraction. (normal =55% -60%)
Heart Failure
 Systolic Heart Failure- decreased ventricle
contraction (most common)
- decreased CO, decreased blood ejected
 Diastolic Heart Failure- decreased ventricle
filling during diastole (older adults and
woman)
- hypertension continued increased workload
- decreased relaxation
SDL– Compare the pathophysiology and clinical manof
causes of the above.
Aetiology of Heart Failure
 Causative factors
 CAD
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MI
Chronic hypertension
Pulmonary hypertension
Valvular heart disease
Cardiomyopathy- disease of
myocardium (viral)
Hyperthyroidism
(thyrotoxicosis)
Congenital Heart Disease
Aetiology of Heart Failure
 Exacerbating/Precipitating Factors
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Anaemia
Infection
Arrhythmias (especially AF)
Some drugs (NSAIDs, Ca2+ blockers, corticosteroids)
Renal dysfunction
Pulmonary embolus
Silent MI /MI ( Affect Contractility )
Excess sodium intake
Transfusions or infusions increasing preload
Poor compliance with current management regime
Pregnancy
Lewis pg 776/895 ( view mechanisms of above)
Definitions
 Cardiac Output = HR (heart rate) X SV (stroke volume)
 Stroke Volume = amount of blood ejected with each heart beat
 Preload: end diastolic filling volume of the left ventricle (EDV)
reflects stretch of the cardiac muscle cells
 Afterload: resistance to ventricular emptying during systole.
(amount of pressure the left ventricle must generate to squeeze
blood into the aorta)
• Myocardial Contractility: the squeezing contractile force that the
heart can develop at a given preload
 Ejection Fraction: indication of the amount of blood ejected with
the contraction
 Frank/Starling Law of the Heart - the heart will contract with
greater force when preload (EDV) is increased
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Clinical Cardiovascular Anatomy & Physiology Concepts, Definitions, & Principles
Green, J. 2003, Texas A&M university 2003 (+ next 2 slides)
Cardiac Output
Cardiac output
http://www.youtube.com/watch?v=0v8-O8P7kw8
Preload and afterload
End Diastolic Volume (EDV)
Volume at the end of diastole
(end of ventricular filling)
End Systolic Volume (ESV)
Volume at the end of systole
(end of ventricular contraction)
Stroke Volume (SV) = EDV - ESV
Ejection Fraction (EF) = SV
EDV
Left ventricular norm: 62%
Ejection Fraction is the
best indicator of heart
performance and
disease prognosis
Starlings Law
Force of heart
contraction
normal
contractility
SV
left
ventricular
performance
d contractility
(heart failure)
preload (EDV)
The heart will contract with greater force when
preload (End Diastolic Volume) is increased
What is happening?
• Dilation – enlargement of heart chambers due to
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elevated pressure over a long time
Hypertrophy – increase in cardiac wall thickness due
to increased workload and CO. Contractility decreased
SNS stimulation : due to decrease in CO.
Neurohormonal response: renin-angiotensin response
– sodium retention- increased peripheral
vasoconstriction – increased arterial BP
ADH secreted due to low CO (Lewis 777/896)
Endothelin production from endothelial cells results in
vasoconstriction
Ventricular remodeling
Counter regulation
 Body’s ability to maintain balance.
 Natriuretic peptides ANP (Atrial) and Btype NP
are hormones produced by heart muscle promoting
venous and arterial vasodilation
 Antagonists of endothelin and aldosterone and
enhance diuresis
 Prolonged distension as in HF leads to a depletion
of these peptides and increased Myocardial
workload
Lewis 778/896
Neurohormonal effect
Cardiac Remodeling
Eccentric hypertrophy
• Volume overload
• Increased CO for
prolonged period
• Cavity dilatation with an
increase in muscle mass
• Ratio between wall
thickness and cavity
remains relatively
constant
Cardiac remodeling
Concentric Hypertrophy
 Chronic pressure
overload (untreated
hypertension) or AS
 Ratio between wall
thickness and cavity
size increases
Heart failure
Heart Failure (Types)
 Left Sided
 Right sided
 Acute/ Chronic ???
SDL Compare left and right sided heart failure with
reference to pathophysiology and clinical
manifestations.
Right and left heart failure
Left and/or Right Sided Failure
 Left Ventricular Failure
 Poor LV function
 Leads to pulmonary congestion
 Right Ventricular Failure
- Left ventricular failure
- Pulmonary Hypertension
- right sided hypertrophy and failure
 Poor RV function
 Leads to increased systemic venous pressure
 Bi-ventricular failure
 Acute Decompensated Heart Failure (ADHF) ( Pulmonary oedema)
Acute and Chronic Failure
 Acute
 MI
 Valvular rupture
 PE
 Drug induced
(cocaine)
 Chronic
 Typically dilated
cardiomyopathy
Downloaded 20 May 07 from
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Congestive Heart Failure
Tests
 CXR
 ECG
 Echocardiography
 FBC – to exclude
anaemia
 Urinalysis
 BUN Creatinine
 Liver function tests
Albumin
 ABG
 Transthoracic
Doppler studies
 BNP
Downloaded 20 May 07 from
http://sprojects.mmi.mcgill.ca/icm_c/Chest/case1/pic1.jpg
NYHA Classification
 Class I: patients with no limitation of ordinary
activities ( ADL’s) - they suffer no symptoms.
 Class II: patients with slight, mild limitation of activity;
they are comfortable with rest or with mild exertion.
 Class III: patients with marked limitation of activity;
they are comfortable only at rest.
 Class IV: patients who should be at complete rest,
confined to bed or chair; any physical activity brings
on discomfort and symptoms occur at rest.
http://www.hcoa.org/hcoacme/chf-cme/chf00070.htm
Clinical Manifestations
 Shortness of breath with or without activity.
 Orthopnea, difficulty breathing while lying flat,
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often pillows are required to sleep.
Low BP- Hypotension
Rapid or irregular pulse.
Edema or swelling of legs, feet and ankles,
abdomen, liver, spleen and lungs.
A chronic dry or frothy cough that may be bloodtinged or resemble foam.
Nocturia, or an increase in urination at night.
Unexplained or unintentional rapid weight gain.
Distended or swollen neck veins.
Clinical Manifestations
 Palpitations, or feeling
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the heart beat.
Loss of appetite or
indigestion.
Cold, diaphoretic
(sweaty) dusky colored
skin.
Oliguria, or decreased
urine output.
Changes in behavior such
as restlessness,
confusion, decreased
attention span and
memory.
Heart Failure
Treatment Strategies for ADHF
Improving left ventricular function by:
• Decreasing intravascular volume
• Decreasing venous return (preload)
• Decreasing afterload
Improving Gas exchange and oxygenation
Improving cardiac function /CO, HR & rhythm
Reducing anxiety
Decreasing progression of disease
Lewis : 901
Management
 Non pharmacological
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General Counselling
Smoking cessation
Vaccination
Prognosis discussion
Activity recommendations
Dietary recommendations > sodium restrictions
Medication counselling
Management
 General Counselling
 Explanation of heart failure and reasons for
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symptoms
Cause of heart failure
Expected symptoms
Action plan if symptoms worsen
Self-monitoring
Treatment plan
Clarification of responsibilities and compliance with
medical plan
Management
Activity recommendations
 Recreation, leisure and work activity
 Sex, sexual difficulties and coping strategies
Dietary recommendations
• Sodium restriction
• Avoid excessive fluid intake
• Fluid restriction if required
• Alcohol restriction
Management
 Medication Counselling
 Effects of medications on quality of life and
survival
 Dosing
 Likely side effects and what to do if they occur
 Coping mechanisms for complicated regimens
 Financial assistance/lower cost meds
Management
 Pharmacological management
 ACE inhibitors > reduce venous pressure
 Diuretics
> Reduce veous pressure and fluid
 ß-blockers > prevent tachycardia
 Calcium channel blockers
 Others
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Spironolactone
Digoxin
Angiotensin II antagonists
Anticoagulation
Aspirin
Nitrates – prevent ischaemiaM
Management
 Prognosis
 Life expectancy
 Advance Directives
 Advice for family in the event of sudden death
 Continuing care and controlling oxygenation
 Physical comfort and psychological suport
Abdominal -Paracentesis
Case study (Lewis 793/912)
LDL
 Read through case study and answer questions
which follow.