Transcript Congestive Heart Failure

Congestive Heart
Failure
Eric J. Milie, D.O.
Objectives:
 Recognize the different causes of right
and left sided heart failure
 Understand the different diagnostic
modalities used to evaluate patients with
heart failure
 Explain the various therapeutic options
available for patients with heart failure
Definition:
A pathopysiologic state characterized by
congestion in the pulmonary or systemic
circulation. It is caused by the heart’s
inability to pump sufficient oxygenated
blood to meet the metabolic needs of the
tissues
Preload:
 Degree of end-diastolic fiber stretch
 For clinical purposes, the end-diastolic
pressure, especially if above normal, is a
reasonable indicator of preload
 Conditions that may effect preload
include: LV dilatation, hypertrophy, and
changes in distensibility or compliance
Afterload
 Force resisting myocardial relaxation
after stimulation from the relaxed state
 Determined by chamber pressure,
volume, and wall thickness at the time of
aortic valve opening
 Clinically, approximates systolic BP at or
neat the time of aortic valve opening and
represents peak systolic wall stress
Frank-Starling Principle
 Degree of end-diastolic fiber stretch
(preload) within a physiologic range is
proportional to the systolic performance
of the ensuing ventricular contraction
 In effect in CHF, but suboptimal response
because the ventricle function is
abnormal
Frank-Starling cont.
The effects of myocardial compliance and contractility on the Frank-Starling
mechanism. Figure reproduced from Internal Medicine, 4th edition, 1994, W.B.
Saunders
Frank-Starling cont.
 If Frank-Starling curve is depressed, fluid
retention, vasoconstriction, and a
cascade of neurohormonal responses
lead to CHF
 Over time, LV remodeling, with
hypertrophy and dilatation further
compromises the heart’s function
Left Ventricular Failure
 Characteristically develops in association
with CAD, HTN, and most forms of
cardiomyopathy and congenital defects
(i.e. VSD, PDA)
Right Ventricular Failure
 Most commonly caused by prior LV
failure ( pulmonary venous pressure and
leads to pulmonary artery HTN) and
tricuspid regurgitation
 May be seen in the face of polycythemia,
overtransfusion, acute renal failure, or
vena caval obstruction
Systolic Dysfunction
 Failure to provide the tissues with
adequate circulatory output
 Most commonly caused by HTN, CAD,
and dilated cardiomyopathy
 More than 20 viruses shown to be causal
Diastolic Dysfunction
 Resistance to ventricular filling (20-40%
of cases)
 Seen in hypertrophic cardiomyopathy,
marked ventricular hypertrophy, and
amyloid infiltration of the myocardium
High Output Failure
 Persistently elevated cardiac output,
resulting in ventricular dysfunction
 Conditions include anemia, beriberi,
thyrotoxicosis, pregnancy, Paget’s
disease, and AV fistula
 Treatment is aimed at the underlying
cause
Etiology:
 Left Ventricular Failure
 Right Ventricular Failure
 Systemic Hypertension
 Valvular Hear Disease (AS,
AR, MR)
 Cardiomyopathy
 Myocarditis
 Bacterial Endocarditis
 Myocardial Infarction
 IHSS
 Valvular Heart Disease (MS)
 Pulmonary Hypertension
 Bacterial Endocarditis (right
sided)
 Right Ventricular Infarction
Clinical Manifestations
 Dyspnea: First on exertion, then with progressively less
strenuous activity
 Orthopnea: Increased venous return in the recumbent
position
 PND: multiple factors
 Nocturnal Angina: Increased cardiac workload, 2º to
increased venous return
 Cheyne Stokes Respiration: Alternating phases of
apnea and hyperventilation
 Fatigue: low cardiac output
 Peripheral Edema
Physical Exam
Left Sided Failure
Right Sided Failure
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• Jugular Venous
Distention
• Peripheral Edema
• Peripheral/ Perioral
cyanosis
• Hepatomegaly
• Ascites
• Hepatojugular Reflux
Pulmonary Rales
Tachypnea
S3 Gallop
Cardiac Murmurs (AS,
AR, MR)
• Paradoxical Splitting of
S2
Assessment of JVD
Shasham, Fadi, and Judith Mitchell, M.D. “Essentials of the Diagnosis
of Heart Failure.” American Family Physician, March, 2001.
Kortakoff’s Sounds with Valsalva
Arterial blood pressure response and Korotkoff's sounds during Valsalva's maneuver. (A)
Sinusoidal response in normal patient. (B) Absent overshoot in patient with heart failure. (C)
Square wave response in patient with heart failure. The red lines indicate when Korotkoff's
sounds are heard. (BP = blood pressure)
Framingham Criteria for Diagnosis of CHF
 Major Criteria
 Minor Criteria
• Paroxysmal Nocturnal
Dyspnea
• Neck Vein Distention
• Rales
• Cardiomegaly
• Acute Pulmonary Edema
• S3 Gallop
• Increased Venous Pressure
• + Hepatojugular reflux
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Extremity Edema
Night cough
Dyspnea on exertion
Hepatomegaly
Pleural Effusion
Vital Capacity ↓ ⅓ from
normal
• Tachycardia (>120bpm)
Major or Minor: Wt loss >4.5 kg over 5 days of treatment
To establish a clinical diagnosis of CHF by these criteria, at least 1 major and 2
minor criteria are required
Diagnosis: CXR Findings
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Cardiomegaly (Cardiothoracic ratio >0.5)
Large Hila with indistinct margins
Prominence of superior pulmonary veins
Fluid in intralobar fissures
Kerley B lines
Alveolar edema
Classic CXR
Echocardiogram
 Two view and Doppler echocardiography
is useful to assess blood flow, global and
left ventricular function, and ejection
fraction
 Transesophageal echo offers higher
quality images, but is invasive and is best
reserved for when the quality of the 2D
images are unacceptable
Echocardiography:
Two-dimensional echocardiogram showing a four-chambers view of the heart
in a patient with systolic dysfunction. Note dilated LV.
Shasham, Fadi, and Judith Mitchell, M.D. “Essentials of the Diagnosis of Heart Failure.” American Family
Physician, March, 2001.
Echocardiography
Two-dimensional echocardiogram showing a four-chambers view of the
heart in a patient with diastolic dysfunction. Note the normal LV size with
hypertrophy.
EKG
 Should be performed on all patients with new diagnosis
of CHF. No specific findings are indicitive of heart
failure, but atrial and ventricular arrhythmias are
common fidings.
 Atrial Fibrillation is found in roughly 25% of individuals
with cardiomyopathy, especially elderly individuals with
advanced failure
 Low voltage with conduction disturbances may be
associated with amyloidosis
Angiography
 Noninvasive method for assessing
systolic and diastolic function
 May be used when echo findings not
consistent with the clinical picture
 Ectopic activity and Atrial Fibrillation may
adversely effect accuracy
B-type Natriuretic Peptide
 New diagnostic test superior to diagnostic
decision making of the primary care physician
 Has reduced clinical indecision from 43-11%
 Median BNP levels in NYHA classes I, II, III,
and IV were 244, 389, 640, and 817 pg/ml,
respectively.
 Values of 50 pg/ml or less had a negative
predictive value of 96%
Maisel, A et al. Rapid Measurement of B-Type Natriuretic Peptide in the Emergency Diagnosis of
Heart Failure. New England Journal of Medicine. 2002 347(3):161-7.
Functional Classification:
New York Heart Association
 Class I: Symptomatic only with greater
than normal activity
 Class II: Symptomatic with ordinary
activity
 Class III: Symptomatic with minimal
activity, asymptomatic at rest
 Class IV: Symptomatic at rest
Treatment
1. Removal of the precipitating cause
2. Correction of the underlying cause
3. Prevention of deterioration of cardiac
function
4. Control of the congestive heart failure
state
Drug Treatment of
Systolic Dysfunction
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Diuretics
ACE inhibitors
ARBs
Β-blockers
Digitalis
Most patients treated with at least two of the
above
Diuretics
Diuretics continued
 Loop diuretics are preferred, usually furosemide by mouth
 In resistant cases, Bumetanide 0.5 – 2.0mg or Metazolone PO
may have additive effects
 Overuse may cause electrolyte imbalances (hyponatremia,
hypomagnesemia, and profound hypokalemia) or volume deficits,
so routine monitoring of serum electrolytes is warranted
 May induce renal failure in some patients
 Adding K sparing diuretics may be used to offset the K-losing
effects of loop diuretics
 Spironolactone may be beneficial in advanced (NYHA Class III or
IV) cases of CHF, decreasing total morbidity and mortality.
Pitt B, Zannad F, Remme WJ, Cody R, Castaigne A, Perez A, et al. The effect of spironolactone
on morbidity and mortality in patients with severe heart failure. Randomized Aldactone
Evaluation Study Investigators. N Engl J Med 1999;341:709-17.
Diuretics cont.
 Clinical efficacy of diuretics is heavily
dependant on dietary sodium restriction
 Log of daily weights should be
maintained ( in greater than 2# needs to
be evaluated)
 No overall decrease in mortality, but relief
of symptoms
Konstam MA. Heart failure: evaluation and care of patients with left-ventricular systolic
dysfunction. Rockville, Md.: U.S. Dept. of Health and Human Services, Agency for Health Care
Policy and Research, 1994; Clinical Practice Guideline no. 11, AHCPR publication no. 94-0612.
ACE Inhibitors
 Peripheral and arterial vasodilatation
 ↓ left ventricular filling pressure at rest
and during exercise
 Favorable effects on remodeling
 Negative inotropic effect on the failing
heart
 Decrease in overall mortality by 25-35%
Effects of enalapril on mortality in severe congestive heart failure. Results of the
Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS). The
CONSENSUS Trial Study Group. N Engl J Med 1987;316:1429-35.
ACE Inhibitors cont.
 Most common side effect is cough (520% of patients) probably 2º to build-up
of bradykinin
 Caution in renal impairment, especially
with concomitant use of diuretics
 ASA reduces the effects of ACE Inhibitors
in CHF patient (inhibits the effects of
kinins)
ARBs
 Theoretically as effective as ACEInhibitors
 No associated cough (no effect on kinins)
 Losartan shown to decrease overall
mortality in patients with heart failure
 No comparison trials (though
ONTARGET is ongoing)
Sharma D, Buyse M, Pitt B, Rucinska EJ. Meta-analysis of observed mortality data from allcontrolled, double-blind, multiple-dose studies of losartan in heart failure. Losartan Heart
Failure Mortality Meta-analysis Study Group. Am J Cardiol 2000;85:187-92.
Hydralazine/ Oral Nitrate
 Used in patients with increased serum
creatinine levels, or those who cannot tolerate
ACEI
 Decrease overall mortality by 25-30%
 Benefit in overall mortality not as pronounced
as in ACEIs, and not as easy to take or tolerate
Cohn JN, Archibald DG, Ziesche S, Franciosa JA, Harston WE,
Tristani FE, et al. Effect of vasodilator therapy on mortality in chronic
congestive heart failure. Results of a Veterans Administration
Cooperative Study. N Engl J Med 1986;314:1547-52.
Digitalis
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Weak inotrope
Blockade of AV Node
Weak vasoconstrictor
Improves renal blood flow
Modestly improves LV function
Lowers dosage needed of diuretics
Reduces need for hospitilization
Digitalis cont.
 Digitalis Investigation Group (DIG) study
showed no decrease in mortality, but
significant reduction in the number of
hospitalizations in patients treated with
digitalis
The Digitalis Investigation Group. The effect on digoxin in mortality and morbidity in patients
with heart failure. N Eng J Med 1997;336:525-533
Digitalis Toxicity
 1st degree AV block, which may progress
to Wenkebach. May also see life
threatening arrhythmias (V. Fib., V. Tach.)
 Nausea, Vomiting, Anorexia, Diarrhea,
Confusion, Amblyopia, and
Xerophthalmia (yellow vision)
Digitalis Effect- EKG
American Society of Consultant Pharmacists, Inc.
β-Blockers
 Increase ejection fraction
 Reduce mortality by roughly 30%, if used
properly
 Improved myocardial function achieved in 6-12
months of therapy
 CIBIS II: Bisoprolol reduced cardiac deaths
and hospitalizations compared to control
The Cardiac Insufficiency Bisoprolol Study II (CIBIS-II): a randomised trial. Lancet
1999;353:9-13.
Heidenreich PA, Lee TT, Massie BM. Effect of beta-blockade on mortality in patients with
heart failure: a meta-analysis of randomized clinical trials. J Am Coll Cardiol 1997;30:27-34
β-Blockers cont.
 Carvedilol (Coreg) is the only β-blocker
specifically labeled for the treatment of
heart failure
 Found to be more effective than other βblockers in patients without ischemic
heart disease
Bonet S, Agusti A, Arnau JM, Vidal X, Diogene E, Galve E, et al. Beta-adrenergic blocking
agents in heart failure: benefits of vasodilating and non-vasodilating agents according to
patients' characteristics: a meta-analysis of clinical trials. Arch Intern Med 2000;160:621-7.
Ca-Channel Blockers
 Use in patients with decreased LV
function has been disappointing
 Some Ca-Channel blockers have
deleterious effect in systolic dysfunction
(Verapimil, Nifedipine, Diltiazem)
Diastolic Dysfunction
Treatment
 May not tolerate reduced volume or blood
pressure (vasodilators, diuretics relatively
contraindicated)
 ACEIs and ARBs may decrease LV mass and
stiffness
 Valve replacement may improve LV function
 Treatment of underlying dominant systolic
dysfunction
Definitive Treatment
 Heart transplant only treatment that potentially
alters the long term course of the disease
 1- and 3-year survival rates 80% & 75%,
respectively
 Dynamic cardiomyoplasty: experimental; wrap
the latissimus dorsi muscle around heart to
stimulate contractility (reported functional
status in 80% of pts, no long term data)
 Implantable ventricular assist devices are
being studied, no long term data at this time
Case Study
Mr. Balaban, a 63-year-old Filipino man, has recently been traveling in the
Philippines. He has a long history of hypertension and usually takes one
aspirin, Lisinopril, and hydrochlorothiazide (HCTZ). He admitted that he ran
out of these when he was traveling. After he returns home, he tells his
daughter that he is "very tired", gets short of breath while walking around the
house, and can't put his shoes on. As he talks with his daughter, she notices
that he is having trouble talking, as if it is hard for him to breathe. She
becomes alarmed and takes him to the emergency room where the
physician finds the following:
- 3+ pitting edema in both ankles
- faint crackles in both lung fields
- extreme fatigue- jugular vein distention when sitting
- moderate shortness of breath
- ten-pound weight gain in the last week- B/P 170/110; pulse 88 and
irregular; EKG shows sinus tachycardia with nonspecific ST/T changes
Question One:
Based on the patient’s presentation in the emergency
department, what would you expect his BNP level to be?
A. 27
B. 250
C. 350
D. 500
E. 775
Answer: E. BNP value for Class III Heart Failure is above 640 pg/ml, Class
IV above 817 pg/ml. Pt getting SOB with walking around the house, talking
on the phone. No mention of dyspnea at rest. Most likely Class III-IV
Question Two:
While under your care, a routine BMP shows the patient to have a
serum Creatinine of 2.3. Which of the following pharmacological
agents will have the greatest benefit towards decreasing this
patient’s risk of mortality?
A. Lanoxin
B. Verapimil
C. Increasing dose of HCTZ
D. Hydralazine/ Isosorbide
E. Nifedipine
Answer: D. VACS trial showed a decrease in the overall mortality in
patients receiving this medication roughly 20-25%.
Question Three:
You evaluate the patient two months after his hospital discharge. He is
complaining of generalized malaise, with nausea and vomiting over the
past two to three days, and has noted things have taken on a yellowish
tint while looking at them over the past week. The family notes that he
has been increasingly confused since his discharge. On physical exam,
the patient has a pulse rate of 72. An EKG recorded in the office shows a
sinus rhythm, with a PR interval of 0.22 and “scooped out” appearing ST
segments. Which of the following medications was the patient most likely
discharged from the hospital on?
A. Lasix
B. Losartan
C. Digoxin
D. Coreg
E. Norvasc
Answer: D. The patients clinical
presentation is classical for digoxin
toxicity/ In addition, the EKG findings of
scooped out ST segments and 1st
degree heart block are commonly seen
on patients treated with digitalis.
Resources:
 Beers, et al. The Merck Manual of Diagnosis and Therapy.
Seventeenth edition. Ch 261. 2004.
 Braunwald, et al. Harrison’s Principles of Internal Medicine.
Fifteenth edition. Pp 1316-1332. 2001.
 Marino, Paul. The ICU Book. Pp 242-246. Rose Tree, Maryland.
1998.