Heart Failure
1 – This is the ability to increase CO during increased
activity
Cardiac Reserve
2 – Decr in pumping ability with consequent decr in
cardiac reserve & adaptive mechanisms that serve to
maintain CO contributes to progression of?
Heart Failure (HF)
3 – HF involves what 2 interactions?
a.
These interactions involve what patho
changes?
1) Decr in pumping ability with decr cardiac
reserve consequently
2) Adaptive mechanisms fail to maintain CO
a.
4 – Define CO
a.
b.
What regulates HR?
What factors affect SV?
LV. dilates
LV. hypertrophy
Neurohormonal stimulation (SNS, RAAS)
V. remodeling
CO = HR x SV
(bpm x how much pumped per beat)
a.
SNS  incr HR
Para NS  decr HR
b.
Preload, afterload & cardiac contractility
5 – This is loading of the heart at the end of diastole /
Volume of blood stretching the resting heart
a. Determined by?
b. Maximum volume of this causes tension in
heart walls which is called what?
Preload
a. Venous return
b. End Diastolic Volume (EDV)
- provides estimate of preload status
- measured clinically
6 – Overstretched ventricles due to extra volume
causes- incr intraventricular pressure, decr SV, &
overstretched muscle fibers- describe what?
a. So what if muscles fibers are overstretched?
(elevated) Preload in HF
7 – What happens overall to preload in HF?
Ventricles are overstretched due to incr volume
- Intraventricular pressure rises
- SV decr
- Muscle fibers overstretch  impaired
pumping & elevates preload even more
8 – Preload = ?
EDV
9 – Impaired pumping action of ventricles can elevate
what?
a. Examples of impaired pumping action:
a.
Impaired pumping/ ejecting blood & preload
elevates
Preload
a. Damage from MI
Dilated cardiomyopathy
Myocarditis
Valvular heart disease
Hypertension
Renal failure with excess circulatory vol.
10 – A pt with preload has impaired ventricle
pumping acting due to what possible causes?
HTN
Renal failure w/ excess vol.
Myocarditis
Valvular heart disease
Dilated cardiomyopathy
MI damage
11 – This is the force that the contracting heart
generates to eject blood from filled ventriclesa. Components include?
Afterload
a. Systemic vascular resistance (SVR)
b. Ventricular wall tension
12 – SVR and Ventricular wall tension are
components to afterload, force that ejects blood from
the heart. What SVR issues lead to afterload
problems?
Aortic stenosis
Arterial HTN
Peripheral vasoconstriction
13 – Ventricular ejection & incr ventricular wall
stress is impaired by what?
Excessive afterload
14 – A pt with an excessive afterload causes
impaired…
Ventricular ejection
Incr wall stress
15 – This is the mechanical performance of the heart-
Cardiac Contractility
16 – A pt’s change in developed tension at a given
resting fiber length, ability of heart muscle to
shorten, pumping, contract & relax, and ability of
contractile elements (actin, myosin) to interact with
& shorten against a load determines what?
Cardiac Contractility
17 – What determines cardiac contractility in a pt?
-Pumping
-Contract & shorten
-Change in developed tension
-Ability of heart muscles to shorten
-Ability of contractile elements to interact/shorten
against a load
18 – What increases CO INDEPENDENT of preload &
muscle strength?
a. What can affect this^
Cardiac contractility
a. Inotropic influence
19 – What causes a +, - Inotropic influence?
(+) Inotropic effect – Sympathetic stimulation
- Digoxin, dobutamine
- Incr strength of contraction
(-) Inotropic effect –Hypoxia, Ischemia
- MI, cardiomyopathy
- Decr contractility
20 – A pt with MI and/or has cardiomyopathy has
which inotropic effect?
Negative, decr contractility
21 – This is an adaptive/compensatory mechanism
used in HF-
Frank-Starling Mechanism
- Supports CO
- Incr SV
22 – Frank-Starling is an adaptive mechanism used in
HF, what does it do/when is it ineffective?
Ineffective when heart is overfilled & fibers
overstretched
-Help support CO
-Incr SV by:
Incr EDV
Incr myocardial fiber stretch
Incr force of next contraction
-Ineffective when heart is overfilled and
overstretched
23 – Compensatory mechanisms try to maintain CO;
What is SNS role in HF to do this?
Elevate catecholamine levels in late stage HF
-E & NE
-Directly stimulates HR & Contractility
-Maintain perfusion (brain, heart, skeletal m.)
Negative aspects:
Incr SVR & Afterload
Decr perfusion in (skin, kidney, abdom. organs)
24 – A pt’s SNS in late stage HF does what?
Elevate catecholamines  E & NE  Directly
stimulates HR & Contractility  Maintain perfusion
of Heart/Brain/& Skel m.
RAAS System effects:
Decr CO  Decr Renal blood flow  Incr Renin secretion from Kidneys w/ Angiotensin II 
Incr Vasoconstriction, Aldosterone & ADH
-
Aldosterone: Incr tubular absorption (retains fluid)
ADH: Vasoconstrict & inhibit h2o release
25 – T/F Adaptive mechanisms don’t work when a pt
has HF
T
26 – This peptide is released from the atria with incr
stretch & pressure that serves to:
- Produce rapid, transient natriuresis, dieresis
and moderate loss of K (body’s diuretic)
- Inhibit adlosteron & rennin secretion
- Antagonist to angiotensin II
- Inhibit release of NE from presynaptic nerve
terminals
Atrial Natriuetic Peptide (ANP)
27 – ANP’s are released in a pt with an incr in stretch
& pressure (such as HF); What do they do following
release?
Produce body’s diuretic components & loss of K
Inhibit aldosterone & renin secretion
Antagonist to angiotensin II
Inhibit release of NE
28 – This is stored in Ventricular cells and functions
similar to ANP’s
a. BNP and ANP are elevated when?
b. When a pt has HF, what levels rise?
Brain Natriuretic Peptide (BNP)
a. HF
b. BNP & ANP
29 – What develops as compensation for an incr
myocardial workload?
Hypertrophy
30 – How does Hypertophy become pathologic?
Structural changes in mass & dilation
Functional changes impair sys & dia.
Hemodynamic overload may develop
Risk for morbidity & mortality
HF in a nutshell –enlarge & can no longer compensate*
31 – Myocytes and Nonmyocytes compose what?
(tissue hypertrophy possible)
Myocardium
32 – Myocardium is composed of:
a. Functional cardiac muscle units, which
growth is limited in cell size not #- called?
b. These are cardiac macrophages/fibroblasts/
vascular smooth muscle/ endothelial cells
that provide support for myocytes; also
capable to incr in cell #
33 – RAAS (angiotensin II) and some SNS drives
what?
a.
b.
Myocytes
Nonmyocytes
Ventricular Remodeling
(refer to slide diagram)
34 – The following are causes of what?
- Mi
- Cardiomyopathy
- Valvular heart disease
- Ischemic heart disease
- Excessive work demand:
HTN, Volume overload, Hypermetabolic
states (hyperthyroidism)
HF
35- A pt with HF may be caused by what?
Excessive work demands (HTN, volume overload,
hypermetabolic states)
-
Accompanied by congestion of body tissues
MI
Valvular heart disease
Ischemic heart disear
Cardiomyopathy
HF
High-Output

Uncommon

Excessive need for CO

Causes:
Severe anemia
Hyperthyroidism
Sepsis
Thyrotoxicosis
Low-Output

Common

Caused by disorders
that impair pumping:
Cardiomypathy
Ischemic heart disease
(IDH)
36 – A pt with an impaired pumping ability due to
cardiomyopathy has which common HF?
Low-output
37 – An excessive need for cardiac output due to
severe anemia, hyperthyroidism, sepsis or
thyrotoxicosis is which kind of HF?
High-output
Systolic
o Impaired pumping/ ejection: EF 55-65%
o Declines progressively with myocardial dysfunction
- Incr diastolic volume, ventricular dilation & wall
tension
-Incr end diastolic pressure
o Decr in cardiac contractility
o Causes:
Impaired Contractile performance
Vol. & pressure overload
Diastolic
o Smaller ventricular chamber size, ventricular
hypertrophy & poor ventricular compliance (@
rest)
o Causes:
Restrict diastolic filling
Incr ventricle wall thickness
Reduce chamber size
Delayed diastolic relaxation
38 – This pt has what dysfunction: ejection fraction of
55%, contractility impaired due to hypoxia (neg
inotropic effect), volume and pressure over load
Systolic dysfunction
39 – A pt with smaller chamber size, ventricular
hypertrophy, and poor ventricular compliance
caused by restricted filling, wall thickness, delayed
relaxation and decr chamber size has which
dysfunction?
Diastolic
Right-side HF
Left-side HF
Venous*
Define
Causes
Accum blood in systemic VENOUS sys. /
congestion in peripheral tissues 
Incr in RA, RVEDP, Systemic Venous Pressures*
-
Persistent Left side failure
Stenosis or regurgitation of tricuspid or
pulmonic valves
RV infarct.
Cardiomyopathy
Cor pulmonae –due to lung disorder
(i.e. severe pneumonia, PE, pulm HTN)
Pulmonary*
Decr CO  Incr LA & LVEDP Pulmonary
Congestion circulation*
Pulmonary capillary filtration pressure > capillary
osmotic pressure = shift of intravascular fluid into
interstitium of lung  Pulmon. Edema
Acute MI (AMI)
Cardiomyopathy
S&S
Fatigue
Dependent edema (both legs)
JVD
Liver engorgement
Ascites
Anorexia + complaints of GI distress (appetite loss)
Cyanosis
Elevation in peripheral venous pressure –fluid
retention
Cyanosis
Blood-tinged sputum
Cough -crackles
Paroxysmal nocturnal dyspnea
Orthopnea
DOE
40 – Incr right atrial pressure (RA), right ventricle
end diastolic pressure (RVEDP) and systemic venous
pressure leads to accumulation?
a. Possible causes?
Accumulation of blood in the venous system,
congestion of peripheral tissues  Right-sided HF
a. Cardiomyopathy
Cor pulmonae
Right ventricular infarction
Stenosis or regurgitation of
tricuspid/pulmonic valves
Persistent Left-side failure
41 – A pt with an AMI and cardiomyopathy would
have a decr in CO, with incr pressures in LA and
LVEDP due to PULMONARY CONGESTION- has
which side HF?
Left-sided HF
42 – What happens in a pt with Right-sided HF?
a. How can it manifest?
Accumulation of blood in venous system
Increased pressures
 Right atrial
 Right ventricular end-diastolic
 Systemic venous
a.
43 – What happens in a pt with Left-sided HF
a. How can it manifest?
Dependent edema, cyanosis, fatigue, JVD,
ascites, peripheral venous pressure elevated,
fluid retention, anorexia, GI distress, loss of
appetite and liver engorgement
Pulmonary Congestion from decr CO
Increased pressures
 Left atria
 Left ventricular end diastolic
Pulmonary capillary filtration is greater than osmotic
 intravascular shift to interstitial  pulmonary
edema
a.
Paroxysmal nocturnal dyspnea, DOE,
cyanosis, blood-tinged sputum, orothpnea
and coughing
Manifestations of HF
Incr capillary pressures –overfill vascular system & venous congestion
Nocturia (later- Oliguria) due to incr in kidneys when asleep
Fluid retention & edema
o
o
Respiratory
Dyspnea –due to pulmonary congestion
DOE
Orthopnea
Paroxysmal Noctural Dyspnea (PND) –sudden attack of SOB while asleep
Chronic, dry, nonproductive cough (worse supine)
Fatigue & ltd’ exercise tolerance
Low LV output
Progressive with incr daily activity
Advanced HF –confusion, memory, anxiety, insomnia
Cachexia & malnourished
Due to
-
Cyanosis –Late sign*
fatigue, malnutrition
Liver & GI congestion –lead to impaired digestion/absorption (bloaty full
feeling)
Circulating toxins & mediators released from poorly perfused tissues
Lips & peripheral extremities
Refer to R & L HF diagram*
Cause
Pulmonary Edema
HF –most common*
 Pulmonary capillary pressures > capillary oncotic
pressures  capillary fluid moves to alveoli  lung
stiffness, difficult expansion  impair gas exchange
Capillary injury
Lymphatic block
Hemoglobin leaves lungs w/o fully oxygenating  SOB, cyanosis
S&S
Life threatening
Gasp for air while seated
Rapid pulse
Moist cool skin -Cyanotic lips & nails
Productive cough of frothy, blood-tinged sputum
Crackles
Worsen: confustion to stupor
Terminal: death rattle –drown in own secretions
44 – A pt has pulmonary edema due to the most
common cause, HF- what is happening in the lungs?
Pulmonary capillary pressures exceed oncotic
pressures
Fluid moves to alveoli
Causing lung stiffness, difficulty expanding 
Impairing gas exchange:
Hemoglobin is leaving lungs w/o fully oxygenating
#1 What manifestations are expected in a pt with
only Left-sided HF?
a. Hepatomegaly
b.
c.
d.
Dependent edema
Pulmonary edema
JVD
C
#2 Manifestations of Right-sided HF?
a. PND
b. Dependent edema
c. Frothy pink sputum
d. Crackles
B
#3 Which of the following puts a pt at risk for Highoutput HF?
a. COPD
b. MI
c. Thyrotoxicocis
d. Restrictive myocardiopathy
C
#4 Left-sided HF EKG shows normal LV EF; What
type of HF is this?
a. Diastolic HF
b. High-output HF
c. Systolic HF
d. Total HF
A