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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

slide6

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.

slide7

HYPER EFFECTIVE

NORMAL

CARDIAC OUTPUT

HYPO EFFECTIVE

END DIASTOLIC PRESSURE

Figure 3: Guyton’s cardiac pump function curve

slide8
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

slide12
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)
slide14
THUS: The adaptive response of reduced

peripheral perfusion secondary to

decrease in cardiac output or

hypovolemia are similar, leading

to worsening cardiac failure.

slide15

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 ACTIVATION ERITHROPOITIN 

WORSENING CF ANEMIA

CARDIAC FAILURE CAN PRESIPITATE ANEMIA AND ANEMIA CAN PRESIPITATE CARDIAC FAILURE

THEN

VISCIOUS CIRCLE OF EVENTS

slide26

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

slide32

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

slide35

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)

slide43

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

slide44

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

slide47

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

slide50

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

slide52

 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)
slide53

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

slide56

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
slide58

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
slide59

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

slide60

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

slide63

CARMEN

LEFT VENTRICULAR DYSFUNCTION AND REMODELLING

  • CARVEDILOL
  • CARVEDILOL AND ENALAPRIL
  • ENALAPRIL

CARVEDILOL AND ENALAPRIL

MORE EFFECTIVE THAN

CARVEDILOL

MORE EFFECTIVE THAN

ENALAPRIL

slide64

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

Carvedilol 1511 1366 1259 1155 1002 383

Metoprolol 1518 1359 1234 1105 933 352

slide65

COPERNICUS

Implications for public health

Lives saved by treating 1000 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

slide67

 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
slide69

ALDOSTERONE RECEPTOR ANTAGONISTS

  • Side effect profile
  • * gynecomastia
  • Eplirinone
  • * Ephesis study
  • * Emphysis study
slide70

ERITHROPOETIN ANALOGS

  • Anemia: CCF
  • DAL Heart Study – ongoing
slide71

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

ad