Cardiac failure
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CARDIAC FAILURE. PROF H duT THERON 2010. MANAGEMENT OF HEARTFAILURE. OVERVIEW Heart failure Resulting from Compensatory mechanisms. Complex syndrome Easily recognized difficult to define. Left ventricular disfunction. systolic diastolic. Inadequate Non specific

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Cardiac failure

CARDIAC FAILURE

PROF H duT THERON

2010


Management of heartfailure

MANAGEMENT OF HEARTFAILURE

OVERVIEW

  • Heart failure

  • Resulting from

  • Compensatory mechanisms

  • Complex syndrome

  • Easily recognized

  • difficult to define

  • Left ventricular disfunction

  • systolic

  • diastolic

  • Inadequate

  • Non specific

  • Worsening cycle of events


Health care impact

HEALTH CARE IMPACT

  • 0,5 to 2% population

  • 200 000 to 800 000 in RSA

  • Adverse prognosis

  • Economic impact

  • 40% five year survival

  • Class 4 NYHA and IHD

  • 43% one year survival

  • 18% three year survival

  • Hospitalization

  • Reduce hospitalization

  • length of stay

  • Pharmacotherapy

  • ACE inhibitors - expensive

  • AIIRB - expensive

  • Loop diuretics - expensive


Definition

DEFINITION

  • Haemodynamic:

    Cardiac failure will result when the heart is unable to effectively manage the volume of blood delivered to the heart.

  • Pathophysiologic:

    Heart failure occurs when an abnormality of cardiac function causes the heart to fail to pump blood at a rate required by the metabolizing tissues or when the heart can do so only with elevased filling pressures. This inability may be due to insufficient or defective cardiac filling and or impaired contraction.

  • Clinical:

    Congestive heart failure represents a complex clinical syndrome characterized by abnormalities of LV function and neurohormonal regulation, which are accompanied by effort intolerance, fluid retention and longevity.


Compensatory mechanisms

COMPENSATORY MECHANISMS

Chamber function adaptive response

PRESSURE

VOLUME

Figure 1: Relationship between end diastolic pressure and end

diastolic volume

NOTE: An increase in end diastolic volume will be accompanied

by an increase in end diastolic pressure


Cardiac failure

CARDIAC OUTPUT

END DIASTOLIC PRESSURE

Figure 2: Starlings cardiac output curve

NOTE: An increase in end diastolic pressure will lead to an

increased cardiac output.


Cardiac failure

HYPER EFFECTIVE

NORMAL

CARDIAC OUTPUT

HYPO EFFECTIVE

END DIASTOLIC PRESSURE

Figure 3: Guyton’s cardiac pump function curve


Cardiac failure

The 3 figures show the following

  • Increased end diastolic volume

    Almost linear related increase in end diastolic pressure

  • Increased end diastolic pressure

    ( increased end diastolic volume )

    Increase in cardiac output

  • Starling

    “ Within physiological limits, the larger the volume of the heart the greater are the energy of its contraction and the amount of chemical change at each contraction.”

    The mechanism is effective only up to a certain point: when cardiac end diastolic volume exceeds a critical level further increases in volume will lead to a reduction in cardiac output. In the failing heart this mechanism ultimately fails to improve myocardial contractility.


Ventricular remodelling

VENTRICULAR REMODELLING

Normal

Regionally ischemic ventricle

Ischemic

Infarcted

Normal

Ischemic

Infarcted

After remodeling


Cardiac failure

VENTRICULAR REMODELLING


Cardiac failure

VENTRICULAR REMODELLING


Cardiac failure

  • Left ventricular dilatation

  • Hypertrophy may occur

  • Fibrosis of infarcted tissue

  • Cardiomegaly

  • Maintain stroke volume

  • Increase in wall stress

  • Increase in myocardial oxygen demand

RESULT

COST


Reflex control mechanisms

REFLEX CONTROL MECHANISMS

Heart failure

Hypovolemia

Decrease in cardiac output

Reduction peripheral perfusion

PERCEIVED THREAT TO CIRCULATORY HOMEOSTASIS

Response

Hypovolemia

Reduced cardiac output

  • Sympathetic nervous system

  • Renin angiotensin

  • Aldosterone

  • Vasopressin (ADH)


Cardiac failure

THUS: The adaptive response of reduced

peripheral perfusion secondary to

decrease in cardiac output or

hypovolemia are similar, leading

to worsening cardiac failure.


Cardiac failure

ABNORMALITIES OF THE SYMPATHETIC NERVOUS SYSTEM

  •  Cardiac output

  •  Peripheral perfusion

  •  Activation sympathetic nervous system

  •  peripheral resistance

  •  afterload

  •  metabolic cardiac demand

  •  cardiac output

VISIOUS CYCLE OF EVENTS


Renin angiotensin aldosterone system

RENIN ANGIOTENSIN ALDOSTERONE SYSTEM

 Cardiac output

 Peripheral perfusion

 Renal perfusion

Angiotensinogen

Renin

Angiotensin 

CONVERTING ENZYME

Angiotensin 

Vasoconstriction

Aldosterone secretion

Increase afterload

Salt & water retention

INCREASE CARDIAC WORKLOAD

WORSENING IN CARDIAC FAILURE


Vasopressin

VASOPRESSIN

Cardiac output

 Baroreceptor pressure

 Hypothalamic blood flow

 Angiotensin 

 Vasopressin

Arteriolar vasoconstriction

Sodium & water retention

Increase afterload

Volume overload

 Cardiac workload

 Cardiac output


Endothelin

ENDOTHELIN

Endothelin levels increased

 Aldosterone

 ANF

 Renin


Atrial natriuretic factor anf

Atrial natriuretic factor (ANF)

Cardiac output

Volume overload

Atrial dilatation

 ANF

 Aldosterone

Vasodilatation

 Neuro endocrine activation

EFFECTIVE COUNTER REGULATORY MECHANISM

ANF - degradation via neutral endopeptidase

Neutral endopeptidase inhibitors   ANF -  RX.CCF


Aldosterone

ALDOSTERONE

 Cardiac output

 Renin angiotensin aldosterone

 Aldosterone levels

 Hypercoagulation?

Na+ retention

Fluid retention

Myocardial fibrosis

LV Hypertrophy

 K+

Arrythmia

Vasoconstrition

Afterload

WORSENING CARDIAC FAILURE

Important implication in pharmacological

relevance for treatment of heart failure

NEW


Result of reflex control mechanisms

RESULT OF REFLEX CONTROL MECHANISMS

  • Increase vascular resistance ( afterload)

  • Salt & water retention ( preload)

 Myocardial wall stress

 Myocardial oxygen demand

CARDIAC FAILURE BEGETS CARDIAC FAILURE


Treatment of cardiac failure

TREATMENT OF CARDIAC FAILURE

Questions

  • Are presenting symptoms and signs related to cardiac failure

  • What is the ethiology

  • Are there precipitating factors

  • Evaluation needed diagnosis: systolic/diastolic

  • How severe is the heart failure syndrome

  • How should the patient be treated acutely

  • How should the patient be treated chronically

  • Medication - ? Detrimental

  • Life style adjustment

  • Surgery


Presipitating factors

PRESIPITATING FACTORS

  • Acute myocardial ischemia

  • Superimposed infections

  • Onset of atrial fibrillation

  • Alcohol abuse

  • Poorly controlled

  • Excessive dietary sodium intake

  • Non compliance with drug therapy

  • Anemia

  • diabetes

  • hypertension

  • hypothyroidism


Role of anemia

ROLE OF ANEMIA

ANEMIA

  • TACHICARDIA

    • INCREASE MYOCARDIAL WORL LOAD

    • WORSENING HEART FAILURE

  • ACTIVATION RAS

    • WORSENING HEART FAILURE

      CARDIAC FAILURE

       RENAL PERFUSION

      RAS ACTIVATIONERITHROPOITIN 

      WORSENING CFANEMIA

      CARDIAC FAILURE CAN PRESIPITATE ANEMIA AND ANEMIA CAN PRESIPITATE CARDIAC FAILURE

      THEN

      VISCIOUS CIRCLE OF EVENTS


  • Cardiac failure

    CARDIAC FAILURE

    AS A RESULT OF

    SYSTOLIC DYSFUNCTION


    Medications commonly used in heart failure treatment protocols

    MEDICATIONS COMMONLY USED IN HEART FAILURE TREATMENT PROTOCOLS

    DRUG

    THIAZIDE DIURETICS

    Hydrochlorothiazide

    Clorthalidone

    THIAZIDE RELATED AGENTS

    Metolazone

    LOOP DIURETICS

    Furosemide

    POTASSIUM-SPARING

    DIURETICS

    Spironolactone

    Triamterene

    Amiloride

    RECOMMENDED

    MAX DOSE (MG)

    50 qd

    50 qd

    10 bid

    240 bid

    100 bid

    100 bid

    40 bid

    MAJOR ADVERSE

    REACTIONS

    Postural hypotension

    Hypokalemia,hyperglycemica,

    rash; rare severe reaction

    includes pancreatitis, bone

    marrow supression, and

    anaphylaxis

    Same as thiazide diuretics

    Same as thiazide diuretics

    Hyperkalemia, gynecomastia

    (spironolactone only)


    Medications commonly used in heart failure treatment protocols1

    MEDICATIONS COMMONLY USED IN HEART FAILURE TREATMENT PROTOCOLS

    DRUG

    SELECT ACE INHIBITORS

    Enalapril

    Captopril

    Lisinopril

    Quinapril

    ANGIOTENSIN II RECEPTOR BLOCKER

    Losartan

    Valsartan

    Candasartan

    BETA BLOCKERS

    DIGOXIN

    HYDRALAZINE

    ISOSORBIDE DINITRATE

    (Isordil)

    ISOSORBIDE MONONITRATE

    (Imdur)

    (Ismo)

    RECOMMENDED

    MAX DOSE (MG)

    20 bid

    100 mg tid

    40 qd

    40 qd

    100 mg qd

    As needed

    100 tid

    80 tid

    240 mg qd

    40 mg qd

    MAJOR ADVERSE

    REACTIONS

    Hypotension, hyperkalemia, renal

    insufficiency, cough, skin rash,

    angioedema, neutropenia, nausea,

    dysgeusia

    Diarrhea, dyspepsia, orthostatic

    dizziness

    Cardiotoxicity, confusion, nausea,

    anorexia, visual disturbances

    Headache, nausea, dizziness,

    tachycardia, lupuslike syndrome

    Headache, hypotension, flushing

    Same as isosorbide dinitrate

    Same as isosorbide dinatrate


    Positive inotropic agents

    POSITIVE INOTROPIC AGENTS

    Digitalis

    • Controversy

    • Digitalis trial

    • Indications

    • Neutral effect on mortality

    • Reduction in hospitalization

    • Atrial fibrillation & CHF

    • Symptomatic CHF despite ACE

    • inhibitors & diuretics

    • Sinus tachycardia related CHF

    • Pregnancy and CHF


    Mild heart failure sinus rhythm

    MILD HEART FAILURE & SINUS RHYTHM

    No AF or tachycardia

    Digoxin

    Not necessary


    Cardiac failure

    INTRAVENOUS INOTROPIC THERAPY

    • Adrenalin

    • Dobutamine

    • Dopamine

    • Milrinone

    • Amrinone


    Diuretics

    Diuretics

    •  peripheral oedema

    •  preload   mycardial wall stress

    •   myocardial oxygen demand

    •   cardiac mechanics

    •   cardiac output

    • Mainstay treatment

    • Relieve volume overload

    • Mild volume overload

    • Severe volume overload

    • Marked volume overload / pulmonary oedema

    • thiazide diuretic

    • loop diuretics

    • intravenous furosamide


    Direct acting vasodilators

    DIRECT ACTING VASODILATORS

    Venodilatation

    Peripheral art. dilatation

     Preload

     Afterload

     Myocardial

    wall stress

     Impedance

     ventricular emptying

     CARDIAC WORK LOAD

     MYOCARDIAL OXYGEN DEMAND

    IMPROVE CARDIAC OUTPUT


    Cardiac failure

    STUDIES

    Isosorhide

    Hydralazin

    Conventional

    therapy

    • V Heft I

    • V Heft II

    • CONSENSUS

    • SOLVD

    • SAVE

    • AIRE

    Enalapril

    Hydralazin

    Enalapril

    Enalapril

    Captopril

    Acute MI

    Ramipril


    Ace inhibitors in heart failure

    ACE inhibitors in heart failure

    • Approximately 7,000 patients evaluated in placebo-controlled clinical trials

    • Consistent improvement in cardiac function, symptoms and clinical status

    • Decrease in all-cause mortality by 20-25% (p<0.001)

    • Decrease in combined risk of death and hospitalisation by 20-25% (p<0.001)


    Angiotesin converting enzyme inhibitors acei

    ANGIOTESIN CONVERTING ENZYME INHIBITORS (ACEI)

     Cardiac output

     Renal perfusion

    Inactive renin

    renin

    Renin substrate (angiotensinogen)

    Angiotensin I

    Angiotensin

    converting Enzyme

    ACE inhibitors

    Angiotensin II

    Pressor effect

    Aldosterone secretion

    Sympathetic stimulation

    Renal action


    Ace inhibitors

    ACE INHIBITORS

    •  Preload

    •  Afterload

    •  Sympathetic outflow

    •  Aldosterone secretion

    Escape later

    Unless contra indicated or tolerated all patients with

    symptomatic heart failure should be treated with an

    ACE Inhibitor.


    Contra indications to ace treatment

    CONTRA INDICATIONS TO ACE TREATMENT

    • Cardiogenic shock

    • Angioneurotic oedema

    • Persistantly elevated potasium level

    • Bilateral renal artery stenosis

    • Pregnancy

    • Absolute

    • Relative

    • Hypotension - systolic BP < 90 mmHg

    • Impaired renal function

    • Hypertrophic obstructive cardiomyopathy

    • Tight AS or MS


    Ace inhibitors contd

    ACE INHIBITORS (CONTD)

    Adverse events

    Predictable in the presence of

    • Hyponatremia

    • Orthostatic hypotension

    • Low BP

    • Renal dysfunction


    Ace inhibitors contd1

    ACE INHIBITORS (CONTD)

    General principles

    • Favorable effects are class related

    • Usually well tolerated

    • Avoid excessive diuresis - lower diuretics

    • Start low dosage

    • Titrate slowly upwards over weeks

    AIM : minimize diuretics dosage

    maximize ACE inhibitors dosage

    Alternatives : Nitrates & Hydralazine


    Ace inhibitors in heart failure1

    ACE inhibitors in heart failure

    Consensus recommendations

    All patients with heart failure due to left ventricular systolic dysfunction should receive an ACE inhibitor unless they have a contraindication to its use or cannot tolerate treatment with the drug

    US Consensus Recommendations (1996)


    Cardiac failure

    ANGIOTENSIN II RECEPTOR BLOCKERS

    Effects = ACE inhibitors

    Data supports use of Losartan / Valsartan /Candesartan

    Indication

    No need to replace ACE for ARII without

    adequate reason

    Possibly no aldosterone escape

    ACE Inhibitor intolerance


    Cardiac failure

    ANGIOTENSIN II RECEPTOR BLOCKERS

    • ELITE 1

      • LOSARTAN : CAPTOPRIL

      • ? REDUCTION IN MORTALITY

    • ELITE 2

      • NO DIFFERENCE IN MORTALITY

    • VALHeFT

      • VALSARTAN : PLACEBO

      • MORTALITY UNAFFECTED

      • REDUCTION IN HOSPITALIZATION

      • IMPROVEMENT IN EJECTION FRACTION

    • CHARM

      • ALTERNATIVE

      • ADDED

      • PRESERVED


    Charm programme

    CHARM PROGRAMME

    3 Component trials comparing candasartan to placebo in patients with symptomatic heart failure

    CHARM

    Alternative

    n = 2028

    LVEF ≤ 40%

    ACE Inhibitor

    intolerant

    CHARM

    Preserved

    N = 3025

    LVEF > 40%

    ACE Inhibitor

    Treated / not treated

    CHARM

    Added

    n = 2548

    LVEF ≤ 40%

    ACE Inhibitor treated

    Primary outcome for each trial: CV death or CHF hospitalisation

    Primary outcome for Overall Programme: All-cause death


    Charm programme1

    CHARM Programme

    Mortality and morbidity

    All Cause Mortality CV Death or CHF Hospitalisation

    Alternative

    Added

    Preserved

    Overall

    0.77

    P = 0.0004

    0.85

    P = 0.011

    0.89

    P = 0.118

    0.91

    0.84

    P < 0.0001

    P = 0.005

    0.7 0.8 0.9 1.0 1.1 1.2 0.6 0.7 0.8 0.9 1.0 1.1 1.2

    Hazard Ratio

    p heterogeneity = 0.37

    Hazard Ratio

    p heterogeneity = 0.43


    Cardiac failure

    INDICATIONS

    SYSTOLIC HEART FAILURE (IMPAIRED FX )

    • ACE INTOLERANCE

    • ? COMBINATION WITH ACE INHIBITORS

    • ISCHAEMIC HEART DISEASE IMPORTANT

    DIASTOLIC HEART FAILURE (PRESERVED FX)

    • NO INDICATION

    NO INDICATION TO REPLACE ACE

    INHIBITORS WITH AR BLOCKERS


    Calcium channel antagonists

    CALCIUM CHANNEL ANTAGONISTS

    • Arteriodilators

    • Negative inotropic effects

    • Nifedepine

    • Diltiazim

    • Verapamil

    Amlodipine well tolerated

    General : Caution in their use

    Limited role


    Beta adrenergic blocking agents

    BETA ADRENERGIC BLOCKING AGENTS

     Beneficial

    • Decrease sympathetic outflow

    • Negative chronotropic effect

    • Negative Inotropic effect

     Beneficial

     Harmfull

    benefit

    In acute myocardial -

    Non ischaemic heart failure -

    ?

    • Metoprolol

    • Bisoprlol

    • Carvedelol

    Benefit proven

    Low dosages

    Titrate slowly

    CAUTION IN THEIR USE


    Cardiac failure

    ADRENERGIC ACTIVATION

    CNS sympathetic

    outflow

    Cardiac

    sympathetic activity

    Sympathetic

    activity to kidneys

    & blood vessels

    b1 receptors

    b2 receptors

    a1 receptors

    Myocyte hypertrophy & death,

    dilatation, ischaemia & arrhythmia's

    Vasoconstriction

    Sodium retention

    Packer, AHA 2000


    Antiadrenergic therapy by blockade

    Antiadrenergic therapy by  blockade

    Sympathetic activation

    b1 receptors

    b2 receptors

    a1 receptors

    Bisoprolol

    Metoprolol

    Propranolol

    Carvedilol

    CARDIOTOXICITY

    Packer, AHA 2000


    Cardiac failure

     BLOCKERS

    • Over 13,000 patients evaluated in placebo-controlled clinical trials

    • Consistent improvement in cardiac function, symptoms and clinical status

    • Decrease in all-cause mortality by 30–35% (p<0.0001)

    • Decrease in combined risk of death and hospitalisation by 25–30% (p<0.0001)


    Cardiac failure

    US Carvedilol Study

    Survival

     blockers in heart failure -

    all-cause mortality

    1.0

    0.9

    0.8

    0.7

    0.6

    0.5

    Carvedilol

    (n=696)

    Placebo

    (n=398)

    Risk reduction = 65%

    p<0.001

    0

    50

    100

    150

    200

    250

    300

    350

    400

    Days

    Packer et al (1996)

    Survival

    Mortality %

    CIBIS-II

    1.00.80.6

    0

    20

    MERIT-HF

    Placebo

    Bisoprolol

    15

    Metoprolol CR/XL

    10

    Placebo

    Risk reduction = 34%

    Risk reduction = 34%

    5

    p=0.0062

    p<0.0001

    0

    0 200 400 600 800

    0

    3

    6

    9

    12

    15

    18

    21

    Months of follow-up

    Lancet (1999)

    Time after inclusion (days)

    The MERIT-HF Study Group (1999)


    Survival effects of b lockers in class iv heart failure

    Survival effects of  blockers in class IV heart failure

    MERIT-HF

    CIBIS II

    BEST

    0.25

    0.5

    0.75

    1.0

    1.5

    2.0

    Favours treatment

    Favours placebo

    Packer, AHA 2000


    Cardiac failure

    Carvedilol provides comprehensive

    adrenergic blockade

    b blockade

    a1 blockade

    Cardiac output

    Renal blood flow

    Worsening heart failure

    a1 blockade

    Sodium retention

    Adapted from M Packer


    Copernicus

    COPERNICUS

    CarvedilolProspective RandomizedCumulative Survival Trial

    Objectives and design

    • To determine the effect of carvedilol compared with placebo on all-cause mortality in patients with severe chronic heart failure

    • Randomised, placebo-controlled, parallel-group multicenter study in patients with ischaemic or non-ischaemic cardiomyopathy


    Cardiac failure

    COPERNICUS

    DSMB recommendations (14 March 2000)

    • Highly significant effect on mortality

    • Exceeded predefined criteria for early termination

    • Consistent across all predefined subgroups

    • Serious adverse events more common on placebo

    • Unanimous recommendation for early termination

    • All patients should be offered open-label carvedilol


    Cardiac failure

    COPERNICUS

    All-cause mortality(recent or recurrent decompensation)

    100

    Carvedilol

    80

    % Survival

    60

    Placebo

    Risk reduction 34%

    P=0.00013

    40

    20

    0

    3

    6

    9

    12

    15

    18

    21

    Months


    Cardiac failure

    COPERNICUS

    Effect of carvedilol on morbidity and mortality

    Death or any

    hospitalisations

    Death or cardiovascular

    hospitalisations

    All patients

    Recent or recurrent

    decompensation

    Death or CHF

    hospitalisations

    0

    0.25

    0.5

    0.75

    1.0

    1.25

    Favours treatment

    Favours placebo

    Packer, AHA 2000


    Capricorn

    CAPRICORN

    CarvedilolPostInfarctSurvivalControlin LeftVentricularDysfunction

    Study characteristics

    • 1958 patients with acute myocardial infarction within 21 days

    • LV ejection fraction <40%, receiving an ACE inhibitor

    • Randomized to placebo or carvedilol (target 25 mg BID)

    • Endpoints: combined risk of death or cardiovascular hospitalisations, all-cause mortality

    • Data analysis ongoing

    Packer, AHA 2000


    Cardiac failure

    SCAN


    Cardiac failure

    CARMEN

    LEFT VENTRICULAR DYSFUNCTION AND REMODELLING

    • CARVEDILOL

    • CARVEDILOL AND ENALAPRIL

    • ENALAPRIL

    CARVEDILOL AND ENALAPRIL

    MORE EFFECTIVE THAN

    CARVEDILOL

    MORE EFFECTIVE THAN

    ENALAPRIL


    Cardiac failure

    COMET STUDY

    CARVEDILOL OR METOPROLOL EUROPEAN TRIAL

    All-cause mortality

    Metoprolol

    Carvedilol

    40

    30

    Mortality (%)

    20

    10

    Time (years)

    0

    0

    1 2 3 4 5

    Number at risk

    Carvedilol15111366125911551002383

    Metoprolol1518135912341105933352


    Cardiac failure

    COPERNICUS

    Implications for public health

    Lives saved by treating1000 patients for 1 year

    HOPE (ramipril)<1

    SOLVD Prevention (enalapril) 7

    SOLVD Treatment (enalapril) 17

    MERIT-HF (metoprolol) 38

    CIBIS-II (bisoprolol) 42

    RALES (spironolactone) 52

    COPERNICUS (carvedilol) 70

    Packer, AHA 2000


    Im plications for publlic health

    IMPLICATIONS FOR PUBLLIC HEALTH

    If 1000 patients are treated per year approximately 70 lives would be saved

    Packer, AHA 2000


    Cardiac failure

     BLOCKERS IN HEART FAILURE

    Consensus recommendations

    All patients with stable class II or III heart failure due to left ventricular systolic dysfunction should receive a  blocker (in addition to an ACE inhibitor) unless they have a contraindication to its use or cannot tolerate treatment with the drug

    Why are the recommendations more restrictive than for ACE inhibitors despite the available evidence?


    Aldosterone antagonists

    ALDOSTERONE ANTAGONISTS

    RALES STUDY (Spironolactone)

    • 30% reduction

    • Class III & IV NYHA CCF

    • Probably a new “old” cornerstone in pharmacological treatment of CCF

    • Reason for benefit

    • Mortality

    • Hospitalizations

    •  Salt & water retention

    •  LVHT & myocardial fibrosis

    •  Arrythmia

    •  Afterload

    • Counter act aldosterone escape with ACEI


    Cardiac failure

    ALDOSTERONE RECEPTOR ANTAGONISTS

    • Side effect profile

    • * gynecomastia

    • Eplirinone

    • * Ephesis study

    • * Emphysis study


    Cardiac failure

    ERITHROPOETIN ANALOGS

    • Anemia: CCF

    • DAL Heart Study – ongoing


    Cardiac failure

    CARDIAC RESYNCHRONIZATION THERAPY

    • Assynchronic right and left ventricular systolic function

    • Right and left ventricular pacing

    • Grade 4 cardiac failure

    • ECG criteria


    Non pharmacological management

    NON PHARMACOLOGICAL MANAGEMENT

    • Avoidance of risk factors

    • Daily fluid allowance

    • Daily salt allowance

    • Rest and activity recommendations

    • Initial bed rest

    • Late supervised / unsupervised

    • training programs


    Surgical management

    SURGICAL MANAGEMENT

    According to

    Operations

    • Ethiology

    • Left ventricular function

    • Coronary bypass

    • Valve repair

    • Valve replacement

    • Congenital lesion surgery

    • Cardiac transplant


    Cardiac failure as a result of diastolic dysfunction

    CARDIAC FAILURE AS A RESULT OF DIASTOLIC DYSFUNCTION

    • Diastoly as important as systoly

    • Incomplete ventricular relaxation

    • Impaired ventricular filling

    • Pulmonary congestion

    • Attempted maintenance cardiac output

    Supernormal ventricular systolic function


    Etiology

    ETIOLOGY

    • Hypertrophic heart disease

    • Ischemic heart disease

    • Old age

    • Infiltrative diseases of the myocardium

    • Hypertension

    • Aortic stenosis

    • Hypertrophic obstructive cardiomyopathy

    • Diffuse low / high grade

    • Myofibrosis


    Clinical profile

    CLINICAL PROFILE

    Systolic dysfunction

    Diastolic dysfunction

     Ventricular relaxation

     Ventricular contraction

    Impaired filling

    Impaired emptying

    Pulmonary congestion

    Dyspnea

    Dyspnea

    HEAVING APEX

    APEX DISPLACED

    LV HYPERTROPHY

    LV DILATATION


    Management

    MANAGEMENT

    Ventricular contraction is normal

    No indication

    Inotropic drugs

    Arteriolar dilators

    Negative chronotropics

    Negative inotropics

     Time ventricular filling

     Ventricular relaxation

    Diuretics

     Pulmonary congestion

    B BLOCKERS

    Ca BLOCKERS

    DIURETICS

    PHARMACOTHERAPY


    General systolic diastolic failure

    GENERAL SYSTOLIC : DIASTOLIC FAILURE

    • Similar symptoms

    • Sometimes similar ethiology

    • Different mechanism of failure

    • Different pharmacotherapy

    HOW TO DISTINGUISH

    Index of suspicion

    Clinical profile  uncertain

    Echocardiography certain


    Cardiac failure

    THANK YOU!


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