Cardiopulmonary I, Hour 119
Tuesday, Feb. 11, 2003
1:00PM
Dr. Michael Smith
Scribed by: Leslie Reddell
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HEART FAILURE
 EXAM 6 TIPS:
o Be sure to go over the Cardiopulmonary Exam 6 Guidelines that Dr. Smith emailed to the class.
 The guidelines are intended to tell you where to focus
 Review the basics of the respiratory physiology
 Spiromety (only relating to obstructive and restrictive diseases)
 Basic blood gas concepts
 Base excess, acid/base, and control of respiration
 Several respiratory questions will be on the exam
-------------------------------------------------------------------------------------------------------------------------------------------------- IMPORTANT NOTE: This is only an introduction to CHF (congestive heart failure). This is a complex
disease process with many variations. This lecture highlights several classic manifestations particularly as
the link to normal Physiology.
o Only classic scenarios will be discussed. We are not taking into account any other diseases
occurring simultaneously with heart failure (not accounting for co-morbidity).
 Co-morbidity = several diseases/disease processes occurring simultaneously
 Heart Failure
o 400,00 new cases of heart failure per year
o Coronary Artery Disease is prevalent (40-70%)
 Often the primary cause of heart failure
o No cure
 A disease you can only manage
 Actually…there is ONE cure = a heart transplant
o Three types of CHF = Right-Sided, Left-Sided, & Biventricular
 Cause for right-sided heart failure ONLY = Pulmonary hypertension
 Chronic afterload for right side
 Left side fine in this case
 Left-sided heart failure is the most common
 Left sided heart failure usually progresses to biventricular heart failure
 Edema
o Edema is the most obvious symptom (general symptom) suggesting heart failure
o Left-sided heart failure = pulmonary edema
 Pulmonary edema is clinically presented as dyspnea (difficulty breathing)
o Right sided edema = peripheral edema
 Neck vein distention = jugular vein distention
 Abdominal Ascites = accumulation of fluid (edema) in the g.i. system
 Results in a big, jiggly belly
 Pitting edema
 Be sure you understand that you will NOT have dyspnea with right-sided heart failure
o Biventricular heart failure = BOTH pulmonary edema & peripheral edema
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 Cause of Left-Sided CHF
o Myocardial Infarction
o Infections
 Heart failure in young individuals is usually due to a prior serious infection
o Coronary Artery Disease (ischemia)
o Valvular Defects (e.g. Aortic stenosis)
o Systemic hypertension
 Sequalae of Heart Failure = the failing of the heart as a pump = not generating enough cardiac output as
demanded by the body
o Pump dysfunction
↓
o Compensatory Responses (you can get compensatory responses without dilation; if no dilation,
then no heart failure)
↓
o Ventricular Dilation (once you get dilation of the heart, you are getting pump dysfunction = failure)
↓
o Exacerbation of Pump Dysfunction
 Time course of Disease
o Acute = can occur immediately
 E.g. as a myocardial infarction occurs
 When a person is having an M.I. they can go into acute heart failure
 Once heart has “healed” (recovered as much as possible after the M.I.), the heart doesn’t
necessarily have to be in a state of heart failure
 Acute heart failure doesn’t necessarily transfer into chronic heart failure
o Often develops within days after serious “injury” to the heart
o Can occur as a result of long-standing insult to the heart
 Due to:
 Hypertension
 CAD = coronary artery disease
 Valve disease
o A GOOD EXAM QUESTION:
 What happens in an acute case of heart failure? How does the system respond?
 Symptoms of Heart Failure
o Fatigue
 CHF persons fatigue very easily
o DECREASED Exercise Capacity
o Dyspnea = left-sided heart failure
o Pulmonary edema = left-sided heart failure
o Venous distension = right-sided heart failure
o Peripheral edema = right sided heart failure
o Tachycardia
 Will see an increased heart rate = trying to compensate for the failing heart
o Increased sympathetic nervous system activity
o Relatively HYPOTENSIVE because not getting enough cardiac output
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 Classification of the Severity of Heart Failure
o Classification is by functional class meaning that it relates to how well the person can function
 Deals with exercise capacity
 Identifies how much a person can function (how much “exercise” a person can do) without
symptoms
o Rated on a I-IV scale with IV being the worse rating
 I = asymptomatic with ordinary physical activity
 This case usually refers to a person who has had an M.I.
 Person is not in heart failure from a functional stand point at this level
 II = ordinary physical activity results in fatigue, palpitations, dyspnea, or angina
 Cannot perform normal-moderate exercise like walking up stairs
 III = marked limitation of physical activity with less than ordinary activity will elicit symptoms
 Very mild exercise, like walking, will evoke symptoms
 IV = patient is symptomatic at rest
 A pressure–volume loop can tell you about the status of the heart failure.
o Loop 1 (dashed lines) = normal PV loop
o Heart Failure Loops = 2 & 3
 Ist evidence of heart failure = accumulation of
fluid = VENTRICULAR DILATION which translates
into INCREASED preload (INCREASED EDV)
 When preload or EDV approaches the limit of
preload reserve, this indicates low ventricular
compliance
o The heart fails to fill anymore because
it is already full and maximally
stretched
 Contractility function also DECREASES in heart
failure = downward shift in contractility
 BUT…due to decreased contractility, the heart tries to compensate by continuing to
increase the preload
 Afterload is INCREASED in heart failure
 ESV is INCREASED in heart failure
 Stroke Volume DECREASES
 Long-standing heart failure
o The heart hypertrophies
 The heart lays down more and more connective tissue DECREASEING the compliance of
the heart
 INCREASES capillary distance (capillaries now further away from myocytes) = O2
diffusion impairment
 The heart becomes stiffer at lower preloads = DECREASED ability to properly fill
 ↑Preload = ↑Afterload
 ↑Systemic Vascular Resistance (due to increased sympathetic activity because of
decreased cardiac output) = ↑Afterlaod
 REMEMBER: Since the heart is failing you DON’T want to increase afterload!
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C.O. AND V.R.
 Cardiac Function Curves
o In the failing heart, the systems tries to expand the blood volume due to the perceived inadequate
cardiac output
o Perceived decrease in the cardiac output causes the
body to volume expand
o The kidney retains fluid (increase blood volume)
Normal
Heart
which leads to an INCREASE in Mean Capillary
Filling Pressure (MCFP)
Abnormal/Failing
Heart
RA PRESSURE
 Pump Dysfunction
o Remember that in CHF, the heart is in a dilated state with increased preload but decreased
contractility which leads to:
 ↑ End-diastolic volume (EDV)
 ↑ End-systolic volume (ESV)
 ↓ Stroke volume (SV)
 ↓ Ejection fraction (EF)
 Pressures in Left-Sided Heart Failure
PRESSURES IN LEFT-SIDED HEART FAILURE:
o REMEMBER that:
 Systolic pressure will be lower in
Mild-Moderate
Severe (Bi-V)
Venous
normal
elevated
the failing heart because the failing
Right
Ventricle
normal
elevated
pump cannot generate enough
Pulmonary
normal/slight ↑
elevated
pressure to produce a normal
Left Atrium
elevated
elevated
cardiac output
Left Ventricle
elevated
elevated
 Pulmonary capillary pressure will
Mean Arterial
normal
normal to ↓
increase due to the back up of
blood = pulmonary edema
 The patient will be hypoxic = ↓PO2, ↑PCO2
 Hypoxia leads to HYPOXIC MEDIATED PULMONARY VASOCONSTRICTION
which INCREASES RIGHT VENTRICULAR AFTERLAOD due to INCREASED
pulmonary artery pressures
 This is the mechanism for causing right-sided heart failure in the left-sided CHF
patient = biventricular heart failure
o A GOOD TEST CONCEPT:
 In severe heart failure you will seen a DECREASE in mean arterial pressure, BUT
you cannot use blood pressure to accurately determine what is going on with a
patient
 There is a wide range of “normal” for blood pressure and you must
compare a patient’s blood pressure to his or her normal pressure
o EX: normal for a particular patient = 160/90, but he/she comes in
with an actual case of heart failure but the same patient now has a
blood pressure of 130/95
 If you did not know the baseline blood pressure for this
patient you could not tell that he/she was in heart failure
based on the blood pressure alone
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The decrease in systolic pressure (compared to the patient’s
normal blood pressure) indicates a reduced stroke volume!
A REDUCTION in pulse pressure also indicates reduce stroke volume because it
is a function of stroke volume and arterial compliance


 Ventricular Dialtion causes:
o Volume Overload
o INCREASED Wall Stress
o INCREASED Work
o INCREASED Energy demands
o DECREASED Ventricular compliance
o INCREASED Connective tissue
o Energy “Starvation” due to increased connective tissue/hypertrophy of the heart
 Compensatory Responses
o Ventricular hypertrophy = INCREASED Cardiac Output
o Increased heart rate = INCREASED Cardiac Output
 Increased CO due to
 ...baroreflex-mediated
 ...impaired parasympathetic control
o Increased sympathetic activity =
 INCREASED Cardiac Output
 INCREASED Systemic Vascular Resistance
 INCREASED Afterload
 Due to altered reflex function
o Decreased β1 - adrenergic receptor sensitivity
 β – receptors become down regulated
 Down regulation of the β-receptors leads to down regulation of the sympathetic nervous
system leading to decreased contractility
 This is a mechanism where the SNS is trying to compensate for itself
 Dampens the effectiveness of the prolonged SNS activity, but still have decreased
cardiac output so the body still tries to continue to increase the sympathetic nervous
system activity
o Increased Renin-Angiotensin = VERY STRONG VASOCONSTRICTION
 INCREASED Volume
 INCREASED Systemic Vascular Resistance
 INCREASED Afterload
o Increased Vasopressin (ADH) = RETAIN VOLUME
 INCREASED Volume
 INCREASED Systemic Vascular Resistance
 INCREASED Afterload
o Net Effect of the Compensatory Responses =
 Increased Blood Volume = INCREASED Cardiac Dilation
 Increased Afterload = DECREASED Stroke Volume & DECREASED Cardiac Output
o NOTE: These compensatory responses are the NORMAL responses, but there is a failing
heart that the system cannot detect. SO…the normal compensatory responses exacerbate
cardiac dilation and the failing pump problems due to the inadequate stroke volume and
perceived hypotension produced by the failing heart.
 Sympathetic nerve activity is chronically elevated in CHF.
o The worse the heart failure, the higher the sympathetic nervous system activity.
o INCREASED plasma catecholamines WORSEN the prognosis of survival!
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 In heart failure, the body has DECREASED inhibitory effects on the Sympathetic nervous system
and INCREASED excitatory effects on the SNS = overall increases in SNS activity
o Decreased Inhibitory SNS Effects due to the Cardiopulmonary Baroreceptors & Arterial
Baroreceptors leads to INCREASED sympathetic nervous system activity
 Respond because they think the body
is HYPOTENSIVE
Decreased
Increased
Inhibitory Effects
Excitatory Effects
 Normally the baroreceptors want to
dampen the effect of the sympathetic
Muscle
Cardiopulmonary
Metaboreceptors
nervous system activity, but this
Baroreceptors
function is impaired in heart failure
Brainstem
o Increased Excitatory SNS Effects due to the
Vasomotor
Neurons
Muscle Metaboreceptors & Arterial
Chemoreceptors leads to INCREASED
Arterial
Arterial
sympathetic nervous system activity
Baroreceptors
Chemoreceptors
o
Sympathetic
Outflow
 Heart failure is a vicious cycle!
o Failure = pump dysfunction = DECREASED cardiac output
o Reduced cardiac output and perceived hypotension leads to neurohumoral stimulation causing
vasoconstriction and volume expansion
o As the system volume expands, the system is at a greater risk
Heart Failure: The Vicious Cycle
for edema
Pump dysfunction
 Left-sided failure = pulmonary edema
 Right-sided failure = peripheral edema
Reduced cardiac output
o The continuous increase in systemic vascular resistance
Increased SVR = afterload
Perceived hypotension
Increased volume = Vent. dilation
(increased afterload) and increased blood volume (leading to
Neurohumoral
ventricular dilation) only INCREASES the pump dysfunction
stimulation
Vasoconstriction
Volume expansion
 Treatment = trying to interrupt the vicious cycle
o For Pump Function
 Inotropic agents
 Digitalis = most common
o Increased contractility without ↑HR
o The work of the heart does not really increase but has increased contractile
function = increased cardiac output
o Digitalis improves the quality of life (the patient can breathe better, function
better, and live with less pain), but it is not beneficial prognostically because it
cannot extend life
 Vasodilators
 Angiotensin Converting Enzyme(ACE) Inhibitor (e.g. Captopril, enalapril, etc..)
 REDUCE AFTERLOAD
o ↓Afterload = ↑Stroke Volume = ↓Preload
o The heart has decreased work due to vasodilation
o For Volume Reduction
 Diuretics (e.g. lasix)
 Diet (i.e. reduce salt intake)
 Diuretics and Diet target congestion
o They decrease preload relieving dyspnea/pulmonary edema in left-side heart
failure or peripheral edema in biventricular/right-sided heart failure