MEDICINE II LECTURE SECTION B 2003

HEART FAILURE (Dra. Aguirre) PAGE 1 OF 8

HEART FAILURE - cerebrovascular accident, congestive

heart failure, left ventricular
- pathophysiologic state in which an enlargement, chronic renal disease
abnormality of cardiac function is - 59% of patients already have TOD at
responsible for the failure of the heart initial consult
to pump blood at a rate …
VALVULAR HEART DISEASE
COMMON CAUSES OF HEART FAILURE - most common cause in the
Philippines is RHD (1 in 1000 of 5-15
1) coronary artery disease
y/o)
2) hypertension
3) valvular heart disease
MYOCARDIUM IN CONGESTIVE
4) cardiomyopathy
HEART FAILURE(CHF)
5) cor pulmonale
6) congenital heart disease
1) mechanical alterations
- decrease in velocity of shortening
PATHOPHYSIOLOGY OF CHF:
- decrease in force development
GENERAL FACTORS
- decrease in the maximum rate of
force development
1) Pressure overload
- little or no change in passive length-
2) Volume overload
tension relationship
3) Loss of muscle
- no change in elastance
4) Decreased contractility
5) Restricted filling
2) biochemical alterations
- decreased actomyosin ATPase
PATHOPHYSIOLOGY OF CHF IN CAD:
activity
- increase in collagen
1) loss of muscle
- decrease in myocardial
2) ischemia
norepinephrine
3) aneurysm (paradoxical expansion,
- decreased function of the
increased wall stress)
sarcoplasmic reticulum
4) increased wall stress of remaining
- ??? decrease in high energy
normal muscle
phosphates
5) mitral regurgitation
- ??? Excess myoplasmic calcium
6) decreased ventricular compliance
- decreased beta-1 adrenergic
receptors
ANATOMY OF CORONARY VESSELS
(review)
MECHANISM OF DYSPNEA IN HF
HEART MUSCLE HYPERTROPHY 1) decreased function
- decreased compliance
TARGET ORGAN DAMAGE (TOD) OF - increased airway resistance
HYPERTENSION 2) increased ventilatory drive
- hypoxemia – PCW

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HEART FAILURE (Dra. Aguirre) PAGE 2 OF 8

- V/Q mismatch – PCW, CO  - thyrotoxicosis

- CO2 production – CO-lactic acidosis - aretrio-venous fistulas
3) respiratory muscle dysfunction - beri-beri
- decreased strength – - Paget’s disease
- endurance - Anemia
- ischemia - Pregnant cardiac

FLUID RETENTION IN HF 6) LOW OUTPUT FAILURE

Caused ultimately in part by:
- decrease in GFR
- by activation of the RAA system
Note: Reduced cardiac output is associated
with:
- decrease in GFR
- increase in renin-angiotensin-
aldosterone leading to Na and H2O
retention
FORMS OF HEART FAILURE
1) ACUTE HEART FAILURE
- largely systolic and the sudden
reduction in cardiac output often result
in systemic hypotension without
peripheral edema
2) CHRONIC HEART FAILURE
- arterial pressure tends to be well-
maintained until very late in the course,
but there is often accumulation of
edema
- Congenital
- Valvular
- Rheumatic
- Hypertensive
- Coronary
- cardiomyopathy
7) SYSTOLIC HEART FAILURE
- inability of the heart to pump
adequate volume of blood and/or to
do so only for an abnormally
elevated filling pressure leading to a
defect in the expulsion of blood
- impaired inotropic state
8) DIASTOLIC FAILURE
- abnormality in diastolic function
leading to a defect in ventricular
filling
- impairment in the ability of the
ventricles to accept blood
- increase in LVEP
PRECIPITATING CAUSES

3) LEFT-SIDED HEART FAILURE 1) reduction in therapy

- LV is mechanicalyl overloaded or 2) high salt intake
weakened leading to pulmonary 3) arrhythmias
congestion 4) systemic infection
5) physical, environmental and
4) RIGHT-SIDED HEART FAILURE emotional stress
- Underlying abnormality affects the right 6) pulmonary embolism
ventricle primarily 7) hypertension
8) cardiac infection and inflammation
5) HIGH OUTPUT FAILURE 9) high output states

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HEART FAILURE (Dra. Aguirre) PAGE 3 OF 8

10)development of an unrelated illness Major or Minor

11)development of a second form of - Weight loss > 4.5kg in 5 days in
cardiac disease response to treatment

SIGNS AND SYMPTOMS For establishing a definite diagnosis of

CHF:
1) PAROXYSMAL NOCTURNAL DYSPNEA 1) 2 major, or
- More specific for heart failure 2) 1 major + 2 minor criteria
- Relates additionally to decreased vital had to be pressent concurrently
capacity and increased blood volume
due to intravascular reabsorption of
peripheral edema during recumbency MAJOR DETERMINANTS OF
CARDIAC OUTPUT
2) Fatigue and decreased exercise
tolerance  myocardial contractility
– second major complex
 cardiac output
FRAMINGHAM CRITERIA FOR HEART
FAILURE  preload  afterload

Major heart rate

- Paroxysmal nocturnal dyspnea or
orthopnea
- Neck vein distention
- Rales
- Cardiomegaly
- Acute pulmonary edema
- S3 gallop
- Increased venous pressure > 16 cm H2O
- Circulation time > 25 seconds
- Hepatojugular reflux
- The major determinants of
cardiac output: increase in all factors
except afterload promote increased
cardiac output
The major determinants of LV
afterload:
Afterload (myocardial wall tension)

Minor Systolic pressure LV radius

- ankle edema
- night cough Impedance to LV LV volume
- dyspnea on exertion ejection
- hepatomegaly
- pleural effusion COMPENSATORY CHANGES
- vital capacity decreased to 1/3 from - increase in:
maximum - preload
- tachycardia >120 bpm - sympathetic tone
- heart rate
- arteriovenous oxygen difference
- circulating catecholamines

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HEART FAILURE (Dra. Aguirre) PAGE 4 OF 8

- RAA TNF-alpha, IL 1-beta/2/6, IFN-

- Arginine vasopressin gamma

 “Failing hearts express elevated

levels of TNF”
Cardiorenal Cardiocirculatory  “Overexpression of this cytokine may
Model Model be one of the several different
maladaptation mechanisms which is
Neurohormonal possible for the progressive cardiac
Model decompensatioon that occurs in
advanced heart failure.
“Cardio-renal”  TNF acts to increase intracellular
- heart failure is a problem of excessive salt levels of tetrahydropterine, which
and water retention that was caused by acts as a cofactor to enhance the
abnormalities of renal blood flow expression of inducible NO
synthase
“Cardio-circulatory or hemodynamic”  The resulting increase in nitric
model oxide (NO) within the heart may
- heart failure was associated with a not only inhibit the contractility of
reduced cardiac output and excessive myocardial cells but also be
peripheral vasoconstriction cytotoxic by virtue of its ability to
trigger apoptosis
“Neurohormonal” model
- cardiac injury causes decreased cardiac
output, subsequent increase in Primary Injury
neurohormonal activation leading to
cytokine release V dysfunction

Vasoconstriction hemodynamic
CYTOKINES – group of relatively small LV remodeling Failure
molecular weight (15-30kDa) pleiomorphic
endogenous peptides produced by a variety Neurohorminal activation
of cell types in response to a variety of
CHF syndrome:
stimuli
Ssx
Inducing stimuli: Morbidity
- systemic inflammatory response Death
- endotoxin effect
- myocardial infarction HELP SAVE HEARTS
- myocarditis (e.g viral)
- transplant rejection APPROACH TO CHF
- congestive heart failure
- cytokines directly implicated in 1) determine etiology
mediating myocardial depressin in 2) determine precipitating causes
systemic sepsis and other forms of 3) assess the severity of HF and
cardiac dysfunction: associated diseases

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HEART FAILURE (Dra. Aguirre) PAGE 5 OF 8

4) assess time course of the disease in Nitrates

light of its natural hx Bypass or
5) assess potential and timing of surgical angioplasty
treatment, if applicable Reduce venous CBV decrease
6) initiate medical treatment: pressure Diuretics
- Reduce work load Na restriction
- Reduce salt intake Venodilators
- ? water restriction (nitrates, ACE-I,
- diuretics morphine)
- digitalis Torniquets
- vasodilators Decrease heart Digoxin in atrial Fib
- new inotropic agents rate Beta blockers
Verapamil,
diltiazem
TREATMENT PRINCIPLES Maintain atrial Cardioversion of
contraction atrial fibrillation
Increased preload Salt restriction, Sequential AV
diuretics, pacing
venodilators
Low CO, increased Arteriolar dilators
systemic resistance
Decreased Postive Inotropic
contractility agents NYHA FUNCTIONAL
Rapid heart rate Increase AV block CLASSIFICATION OF HEART
- atrial fibrillation Improve LV FAILURE
- sinus performance (beta-
tachycardia blockade) Class I:
- No limitation
TREATMENT OF DIASTOLIC - Ordinary physical activity does not
DYSFUNCTION cause undue fatigue, dyspnea, or
palpitation
GOAL OF TX METHOD
Reduce Anti-HPN Class II:
hypertrophy Surgery (ex. AVR - Slight limitation of physical activity
progression for aortic stenosis) - Such patients are comfortable at rest
Improve Systemic unloading - Ordinary physical activity results in
ventricular Ischemia fatigue, dyspnea, or palpitation
relaxation treatment
Calcium channel Class III:
blockers - Marked limitation of physical activity
Prevent ischemia Beta-blockers - Althought patients are comfortable
Calcium channel at rest, less than ordinary activity will
blockers lead to symptoms

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HEART FAILURE (Dra. Aguirre) PAGE 6 OF 8

Class IV: - furosemide (loop) + aldosterone

- inability to carry on any physical activity (DistalCT) – good combination – act
without discomfort. Symptoms of CHF on different sites so can complement
are present even at rest each other
-
Asympto- With ssx severe refractory ACE INHIBITORS
matic - first drug top have serious effect on
ACE INHIBITORS survival in severe heart failure
NA RESTRICTION - has been shown to postpone onset
4g 2 grams of heart failure in symptomless
1-2 L fl subjects with LV dysfunction
restrxn - if carefully titrated in combination
BETA BLOCKERS treatment with adrenoreceptor
DIGOXIN blockade has been proben effective
DIURETIC in carefully selected patients
TAILORED - blocks conversion of angiotensin I to
COMBINATION II, thereby blocking A II’s effects of
TRaNSPL; vasoconstriction and increased
ASSTDEV. aldosterone secretion

I II III IV BETA-BLOCKERS
ACEI ::::::::::::::::::::::::::::::::::::: - CIBIS
::::::::::::::::::::::::::::::::::: - MERIT (metoprolol) – decreased
NA ::::::::: death by 34%, cardiovascular death
INTAKE ::::::::::::::::::::::::::::: by 38%, sudden death by 41%, and
REST ,.,.,.,.,.,::::::::: CHF death by 49%
:::::::::::::::::::::::::::::
DIGOXIN ::::::::::::::::::::::::::::: Lessons from ACE-I trials in heart
::::::::::::::::::::::::::::: failure
DIURETI :::::::: - ACE-I exert their major effects not
CS ::::::::::::::::::::::::::::: through vasodilation but through
INOTROPI :::::::: blocking of neuroendocrine
CS (IV) :::::::::::::::::: activation
- Neuroendocrine activation is
SPCL ::::
MEAS. ::::::: associated with improved rognosis
and therapeutic effect
- ACE-I therapy improves survival in
DIGOXIN – prevents worsening of HF
pateints with heart failure and
systolic dysfunction.
DIURETICS
- effective in controlling symptoms and
IMPROVEMENT IN NYHA CLASS AND
edema
QUALITY OF LIFE IN MERIT-HT
- no effect on survival once heart failure
- majority improved
is apparent
- McMaster overall evaluation score

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HEART FAILURE (Dra. Aguirre) PAGE 7 OF 8

- Beta-blockers improved survival in CAUSES OF SYSTOLIC

patients with mild to moderate (and DYSFUNCTION
perhaps, advanced) HF UNDERLYING Rhythm observed
- Decreased hospitalization CAUSE
- Improved QOL and reduction of Acute myocardial V. tach (usu
symptoms ischemia or polymorphic) or
infarction (CAD or VF, bradycardia,
CONCLUSIONS: embolus) EMD
- -blockers improve survival in patients Pulmonary Bradycardia, EMD
with mild to moderate (and perhaps embolism
advanced) heart failure Embolic/hemorrha Bradycardia,
- -blockers reduce hospitalization gic stroke polymorphic VT
- -blockers improve quality of life and Drug prolonging
reduce symptoms QT interval
- Electrolyte Polymorphic VT
CONDITIONS WARRANT HEMODYNAMIC depletion (K, Mg)
MONITORING Hyperkalemia Bradycardia
- hypoperfusion suspected from: Apparent VT
- narrow pulse pressure Exaggerated vagal Sinus bradycardia
- cool extremities reflexes Complete heart
- mental obtundation block
- decreased renal function with Primary arrhythmia VT, VF
volume overload - ventricular Sinus bradycardia
- marked hyponatremia tachyarrhythmi Complete heart
- congestion with: as block
- angina or other evidence of active - conduction
ischemia system disease
- Hemodynamically significant
arrhythmia VENTRICULAR FIBRILLATION
- persistent systematic hypotension - looks like a bag of worms
during ACEI tx
- baseline renal impairment TRIAGE – a French word meaning to
- severe intrinsic pulmonary disease pick or to sort according to quality, thus
- persistent congestion despite the it refers to ALLOCATING RESOURCES
following: FOR THE SHORTEST TERM
- salt and fluid restriction
- high-dose loop diuretics - recently, TRIAGE – have a wider
- Metolazone or a thiazide significance, applying to any situatin
- Evaluation for heart ransplant for where patients must be selected for
advanced heart failure the immediate treatment because
limited resources dictate that not all
can be given equal treatment

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HEART FAILURE (Dra. Aguirre) PAGE 8 OF 8

DIFFICULTY IN TRIAGE – CHOICE

BETWEEN:

I. FEW patients with expensive and

lengthy treatment which may keep
them alive with restricted activity
VERSUS
LARGER number of patients with simpler
treatment which may keep them normally
active for many years (vaccine, dietary
suuplement, preventive measures)

II. Benefit for the few is small

VERSUS
Benefit for the many is great

However, for each of those few, the need is

very great indeed!… and the benefit from
their point of view is real

Heart transplantation is an extraordinary

means… therefore, it is NOT obligatory

A doctor…
cure sometimes,
palliates oftentimes,
comforts/consoles always….

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