Heart Failure - PowerPoint PPT Presentation


PPT – Heart Failure PowerPoint presentation | free to download - id: 1effa-MGY4Z


The Adobe Flash plugin is needed to view this content

Get the plugin now

View by Category
About This Presentation

Heart Failure


Symptomatic heart failure has a worse prognosis than most cancers, with a one ... overload, 'heart failure' is generally preferred to 'congestive heart failure' ... – PowerPoint PPT presentation

Number of Views:1069
Avg rating:3.0/5.0
Slides: 54
Provided by: VictoriaS2


Write a Comment
User Comments (0)
Transcript and Presenter's Notes

Title: Heart Failure

Heart Failure
  • Bill Wolf
  • Edited from Vicki Shanmugam, Bob Rabbani and
    Navreet Sandhu

  • Defined as a pathophysiological state in which
    an abnormality of cardiac function is the cause
    of the heart to pump blood at a rate that is not
    able to keep up with the needs of the body.

Heart Failure
  • 5 million Americans with heart failure today
  • 6-10 of people older than 65 yo have it
  • 500,000 are diagnosed with HF each year
  • Reason of at least 20 of all hospitalizations
    (6.5 million hospital days each year)
  • Over past decade, rate of hospitalization has
    increased by 159 (550,000 to nearly 900,000 per
  • Symptomatic heart failure has a worse prognosis
    than most cancers, with a one-year mortality of
    almost 45
  • Thus, we have a strong incentive to identify,
    predict, and treat the factors contributing to

Heart Failure
  • Heart failure is a clinical syndrome arising from
    any structural or functional cardiac disorder
    that impairs the ability of the ventricle to fill
    with or eject blood. Because not all patients
    have volume overload, heart failure is
    generally preferred to congestive heart failure

Two types of heart failure
  • Systolic
  • EFon CXR, S3
  • Assoc with previous MI, HTN, DM, sleep apnea
  • Diastolic
  • EF40, LV hypertrophy, Congestion without
    cardiomegaly on CXR, S4.
  • Assoc with HTN, DM, Obesity, COPD, dialysis

Diastolic Heart Failure
  • Associated conditions include
  • Restrictive (infiltrative) cardiomyopathy
  • Amyloidosis
  • Sarcoidosis
  • hemochromatosis
  • Obstructive and nonobstructive hypertrophic
  • Pericardial constriction
  • LVH from HTN

Characteristics of Patients with Diastolic Heart
Failure and Patients with Systolic Heart Failure
Jessup, M. et al. N Engl J Med 20033482007-2018
Diastolic Failure
  • Diagnosis often made by clinician who recognizes
    the typical signs and symptoms
  • Relatively little evidence to guide care of
    patients with this condition
  • Patients are treated with risk factor
    modification, controlling blood pressure, heart
    rate, ischemia, and volume

Systolic Heart Failure
  • Coronary artery disease is the cause in 2/3 of
  • Other causes include
  • HTN
  • Thyroid disease
  • Valvular disease
  • Alcohol
  • Myocarditis
  • No identifiable cause (i.e. idiopathic dilated

Heart Failure as Progressive Disorder
  • Ventricular dysfunction begins with injury or
    stress to the myocardium, and progresses
  • The heart chamber generally dilates,
    hypertrophies, and becomes spherical (remodeling)
  • This increases the hemodynamic stress on the
    walls of the heart

  • Left ventricular remodeling involves mechanical,
    neurohormonal, and genetic factors that alter the
    ventricular size and function
  • Patients with HF have elevated levels of
    norepinephrine, angiotensin II, aldosterone,
    endothelin, vasopressin, and cytokines
  • Remodeling occurs in several conditions,
    including myocardial infarction, cardiomyopathy,
    hypertension, valvular heart disease
  • One sees hypertrophy, myocyte death, and
    increased interstitial fibrosis

Ventricular Remodeling after Infarction (Panel A)
and in Diastolic and Systolic Heart Failure
(Panel B)
Jessup, M. et al. N Engl J Med 20033482007-2018
Consequences of Remodeling
  • Mitral Regurgitation
  • Arrhythmias and Bundle Branch Block

Mitral Regurgitation
  • As the left ventricle dilates and the heart
    becomes globular, the papillary muscles and
    mitral leaflets change orientation, leading to
    distortion of the papillary apparatus
  • Mitral regurgitation results in volume overload
    on an overburdened ventricle, further causing
    progression of disease

  • Another consequence of ischemia, inflammation,
    fibrosis, and aging is arrhythmia
  • SVT, especially a. fib., often marks the onset of
    systolic or diastolic heart failure
  • In patients with HTN or abnormal myocardial
    function, elevation in ventricular end-diastolic
    volume leads to atrial stretch, which in turn
    causes electrical instability

  • Abnormal myocardial conduction can also lead to
    left bundle branch block, which is a predictor of
    sudden death
  • LBBB causes abnormal ventricular activation and
    contraction, ventricular dyssynchrony, delayed
    opening and closure of the aortic and mitral
    valves, and abnormal diastolic function
  • LBBB can result in reduced ejection fraction,
    cardiac output, and arterial pressure, and
    paradoxical septal motion, increased LV volume,
    and mitral regurgitation

  • Rate of sudden cardiac death in patients with
    heart failure is 6-9 times that in the general

  • Typically will present with symptoms of
  • Dyspnea on exertion
  • Orthopnea
  • PND
  • Ankle swelling
  • Weight gain
  • Sometimes abdominal distension
  • Tiredness and weakness

Special Questions to ask
  • Chest pain or exertional angina strongly
    suggests IHD as cause
  • Recent flu like illness consider viral
  • History of longstanding alcohol or HTN consider
    alcoholic or hypertensive cardiomyopathy
  • History of proteinuria or chronic inflammatory
    condition, consider amyloid
  • Recent blood transfusion or Sx consider volume
  • FHx, along with diabetic bronzed pt consider
    hereditary hemochromatosis.
  • Things that worsen underlying heart failure
  • Antiarrhythmics disopyramide and flecanide
  • Ca channel blockers esp. Verapamil
  • B Blockers

Physical exam look specifically for evidence of
how bad their HF is and clues to the underlying
  • Sympathetic overdrive (to compensate for low CO)
    evidenced by sinus tachycardia, diaphoresis,
    and peripheral vasoconstriction
  • Pulsus alternans alternating strong and weak
    peripheral pulses, exact pathophysiology not
  • Manifestations of volume overload
  • JVP
  • Pleural effusions, alveolar edema crackles
  • Peripheral edema
  • Ascites, hepatomegaly, splenomegaly
  • Ventricular enlargement displaced PMI
  • S3 or S4
  • Pulmonary hypertension complaints of chest
    pain, palpable pulmonic tap, pulmonary

  • CBC R/o anemia as ppt.
  • Chem 7 assess BUN/Creat/K
  • LFT may rise with hepatic congestion
  • Fasting glucose screen for DM
  • TFT r/o thyrotoxicosis or hypothyroidism
  • Fe/TIBC if hemochromatosis is a risk
  • BNP -- 100 is 90 sensitive for HF, equally as
    predictive as finding cardiomegaly on CXR, or
    rales on clinical exam. Cost only 20

  • Cardiomegaly
  • Prominent upper lobe vessels
  • Kerley B lines
  • Pleural effusions
  • Bats wing pulmonary edema

(No Transcript)
(No Transcript)
EKG and Echo
  • EKG
  • Look for arrhythmias e.g. A fib, V Tach
  • Conduction abnormalities esp. seen in pts with
    dilated cardiomyopathy
  • Echo
  • EF helps distinguish systolic and diastolic HF
  • Regional wall motion abnormalities suggesting
  • Valvular disease
  • Pulmonary artery pressures.

Framingham Criteria
  • 2 major
  • 1major and
  • 2 minor

NYHA (functional classes)
ACC/AHA Stages of heart failure
  • Staging introduced to get people to realize
    that there is an element of preventability in HF
    and that pts need screening while asymptomatic in
    order to prevent progression (just like cancer

Stages of Heart Failure
  • Examples of patients in each stage
  • Stage A patients with HTN, CAD, DM, history of
    cardiotoxic drug therapy or alcohol abuse, h/o
    rheumatic fever, FHx of cardiomyopathy
  • Stage B LVH or fibrosis, LV dilatation or
    hypocontractility, asymptomatic valvular heart
    disease, previous MI
  • Stage C dyspnea or fatigue due to LV systolic
    dysfunction, asymptomatic pts undergoing tx for
    prior sx of HF
  • Stage D pts frequently hospitalized for HF and
    can not be safely d/c ed from hospital, pts in
    hospital awaiting transplant, pts at home
    receiving IV inotropes or LVAD, pts in hospice

How do you manage this patient?
  • ASA
  • B-Blocker
  • ACE
  • Spirnolactone
  • Lasix
  • Nitrates
  • Hydralazine

Heart Failure
  • Large trials have looked at the effects of ACE
    inhibitors, angiotensin receptor antagonists,
    beta-blockers, spironolactone, biventricular
    pacing, CABG, and the use of multidisciplinary
    teams. All have been shown to reduce rates of
    hospitalization and improve functional status.

Stage A Heart Failure
  • Treat risk factors!
  • Treatment of hypertension decreases incidence of
    left ventricular hypertrophy and cardiovascular
    mortality and reduces incidence of heart failure
    by 30-50
  • Use of ACE inhibitors in asymptomatic high-risk
    patients with DM or vascular disease reduces rate
    of death, MI, and stroke
  • Use of ARBs (losartan) has delayed the first
    hospitalization for heart failure in patients
    with DM and nephropathy
  • Goal of treatment is to prevent remodeling!

Stages B, C, and D Heart Failure
  • Goals of those with low ejection fraction are to
    slow progression of disease and alleviate
  • Lifestyle modification remains a mainstay, for
  • Moderate sodium restriction
  • Weight monitoring
  • Medication regimen compliance
  • Moderation of alcohol
  • Exercise program for selected patients

Stages B, C, and D Heart Failure
  • ACE inhibitors limit the physiologic consequences
    of angiotensin II levels, and decrease
    degradation of bradykinin (which promotes
    vasodilation and natriuresis in the kidney)
  • ACE inhibitors after an MI improve survival,
    rates of hospitalization, symptoms, cardiac
    output and promote reverse remodeling
  • Optimal target dose of ACE inhibitors is not
    clear, with trials showing low and high doses as
    having similar effects on mortality
  • Not certain whether any difference among the many
    different ACE inhibitors out there today

Stages B, C, and D Heart Failure
  • Beta-blockers counteract the effects of the
    sympathetic nervous system during heart failure
  • Beta-blockers improve survival, morbidity,
    ejection fraction, remodeling, quality of life,
    rates of hospitalization, and incidence of sudden
  • Should be used in select patients who are not
  • In those with asthma, DM with frequent
    hypoglycemia, and bradycardia /- heart blocks
    should use caution

Stages B, C, and D Heart Failure
  • With beta-blockers one sees improvement in
    systolic function even after 3 mos, with reversal
    of remodeling after 4 mos
  • Carvedilol (nonspecific beta-blocker with alpha
    effects) and metoprolol (beta-1 selective with no
    alpha effects) are approved for the treatment of
    heart failure, but the most prescribed med is

Stages B, C, and D Heart Failure
  • ARBs should be used for those who can not
    tolerate ACE inhibitors, with trials showing that
    ARBs have similar efficacy in heart failure to
    ACE inhibitors

Stage C and D Heart Failure
  • Spironolactone, which blocks deleterious effects
    of increased aldosterone (salt retention,
    hypertrophy, etc), has been shown to be helpful
    in patients with NYHA class III or IV symptoms

Stage C and D Heart Failure
  • Diuretics are used to control congestion
  • Thiazide or loop diuretics often prescribed, and
    combination therapy may be helpful in advanced
  • Digoxin has no improvement in mortality, but
    reduces rates of hospitalization and worsening
    heart failure

Stage C and D Heart Failure
  • Biventricular pacemakers (where one lead is in
    the right ventricle and the other is passed
    through the right atrium, through the coronary
    sinus, and into a cardiac vein on the lateral
    wall of the left ventricle) improves ventricular
  • The pacemaker can be used to treat patients with
    heart failure and a wide QRS
  • Effects include reverse remodeling (leading to
    decreased heart size, improved EF, and decreased
    mitral regurgitation)
  • Exercise tolerance improves, as does quality of
    life, and rate of hospitalization
  • Has not been shown to enhance survival

Stage C and D Heart Failure
  • Revascularization (either PCI or CABG)
  • Improves symptoms
  • Improves cardiac performance
  • Reduces risk of sudden death
  • Mechanical devices (e.g. LVADs) are continuing to
    evolve for patients awaiting heart
    transplantation or as destination therapy

AHA/ACC Recommendations
  • The following classification system has been used
    by the AHA/ACC
  • Class I conditions for which there is evidence
    and/or general agreement that a given
    procedure/therapy is useful and effective
  • Class II conditions for which there is
    conflicting evidence and/or a divergence of
    opinion about the usefulness/efficacy of
    performing the procedure/therapy
  • Class III conditions for which there is evidence
    and/or general agreement that a procedure/therapy
    is not useful/effective and in some cases may be

Specifically ACE Inhibitors
  • Class I AHA/ACC recommendations
  • Stage A patients with a history of
    atherosclerotic vascular disease, DM, or HTN and
    associated CV risk factors
  • Stage B patients with recent or remote history of
    MI regardless of EF
  • Stage B patients with reduced EF, whether or not
    they have experienced an MI
  • In all Stage C and D patients unless

ACE inhibitors
Specifically Beta-Blockers
  • Class I AHA/ACC recommendations
  • Stage B patients with recent MI regardless of EF
  • Stage B patients with reduced EF, whether or not
    they have experienced an MI
  • Stable Stage C and D patients. They should have
    no or minimal evidence of fluid retention and
    have not recently required positive inotropic

Relative contraindications for B-blocker use
  • HR
  • Systolic
  • Signs of peripheral hypoperfusion
  • PR interval0.24
  • Second or third degree heart block
  • Severe COPD
  • Asthma history
  • PVD

Specifically Spironolactone
  • Low doses of spironolactone given with an ACE
    inhibitor in patients with class IV symptoms
    reduced the risk of death and hospitalization
  • Class IIa recommendations
  • Spironolactone in Stage C patients with recent or
    current Class IV symptoms, preserved renal
    function and a normal potassium concentration

Specifically ARBs
  • They should be considered instead of ACE
    inhibitors due to intolerance.
  • Class IIa recommendations
  • In Stage C patients who are being treated with
    digitalis, diuretics, and a beta-blocker who
    cannot be given an ACE inhibitor because of cough
    or angioedema

Specifically diuretics
  • Class I indications
  • In Stage C and D patients who have evidence of
    fluid retention
  • In diastolic failure to control pulmonary
    congestion and peripheral edema

(No Transcript)
About PowerShow.com