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Low-Output Heart Failure Systolic Heart Failure (HFREF): Decreased Left ventricular ejection fraction Diastolic Heart Failure (HFPEF): Elevated Left and Right ventricular end-diastolic pressures Normal LVEF High-Output Heart Failure

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slide2
Low-Output Heart Failure
    • Systolic Heart Failure (HFREF):
        • Decreased Left ventricular ejection fraction
    • Diastolic Heart Failure (HFPEF):
        • Elevated Left and Right ventricular end-diastolic pressures
        • Normal LVEF
  • High-Output Heart Failure
        • Seen with peripheral shunting, low-systemic vascular resistance, hyperthryoidism, beri-beri, carcinoid, anemia
        • Often have normal cardiac output
  • Right-Ventricular Failure
        • Seen with pulmonary hypertension, large RV infarctions.
causes of low output heart failure
Causes of Low-Output Heart Failure
  • Systolic Dysfunction
      • Coronary Artery Disease
      • Idiopathic dilated cardiomyopathy (DCM)
          • 50% idiopathic (at least 25% familial)
          • 9 % myocarditis (viral)
          • tachycardia, peripartum, hypertension, HIV, connective tissue disease, substance abuse (alcohol), doxorubicin/herceptin
      • Hypertension
      • Valvular Heart Disease
  • Diastolic Dysfunction
      • Hypertension
      • Coronary artery disease
      • Hypertrophic obstructive cardiomyopathy (HCM)
      • Restrictive cardiomyopathy
mal adaptation neurohormonal
(Mal) adaptation-neurohormonal
  • Activation of the sympathetic nervous system
    • Vasoconstriction/increased afterload
    • Tolerance
    • Arhythmogenic
slide6
Activation of renin-angiotensin system
    • Na resorption
    • Vasoconstriction
    • Apoptosis/fibrosis
slide7
Antidiuretic hormone
  • Proinflammatory cytokines
    • TNFalpha
    • IL-6
clinical presentation of heart failure
Clinical Presentation of Heart Failure
  • Due to excess fluid accumulation:
    • Dyspnea (most sensitive symptom)
    • Edema
    • Hepatic congestion
    • Ascites
    • Orthopnea, Paroxysmal Nocturnal Dyspnea (PND)
  • Due to reduction in cardiac ouput:
    • Fatigue (especially with exertion)
    • Weakness
slide9
S3 gallop
        • Low sensitivity, but highly specific
  • Cool, pale, cyanotic extremities
        • Have sinus tachycardia, diaphoresis and peripheral vasoconstriction
  • Crackles or decreased breath sounds at bases (effusions) on lung exam
  • Elevated jugular venous pressure
  • Lower extremity edema
  • Ascites
  • Hepatomegaly
  • Splenomegaly
  • Displaced PMI
      • Apical impulse that is laterally displaced past the midclavicular line is usually indicative of left ventricular enlargement>
lab analysis in heart failure
Lab Analysis in Heart Failure
  • CBC
        • Since anemia can exacerbate heart failure
  • Serum electrolytes and creatinine
        • before starting high dose diuretics
  • Fasting Blood glucose
        • To evaluate for possible diabetes mellitus
  • Thyroid function tests
        • Since thyrotoxicosis can result in A. Fib,

and hypothyroidism can results in HF.

  • Iron studies
        • To screen for hereditary hemochromatosis as cause of heart failure.
  • ANA
        • To evaluate for possible lupus
  • Viral studies
        • If viral mycocarditis suspected
laboratory analysis cont
Laboratory Analysis (cont.)
  • BNP
        • With chronic heart failure, atrial mycotes secrete increase amounts of atrial natriuretic peptide (ANP) and brain natriuretic pepetide (BNP) in response to high atrial and ventricular filling pressures
        • Usually is > 400 pg/mL in patients with dyspnea due to heart failure.
chest x ray in heart failure
Chest X-ray in Heart Failure
  • Cardiomegaly
  • Cephalization of the pulmonary vessels
  • Kerley B-lines
  • Pleural effusions
cardiac testing in heart failure
Cardiac Testing in Heart Failure
  • Electrocardiogram:
    • May show specific cause of heart failure:
        • Ischemic heart disease
        • Dilated cardiomyopathy: first degree AV block, LBBB, Left anterior fascicular block
        • Amyloidosis: pseudo-infarction pattern
        • Idiopathic dilated cardiomyopathy: LVH
  • Echocardiogram:
    • Left ventricular ejection fraction
    • Structural/valvular abnormalities
further cardiac testing in heart failure
Further Cardiac Testing in Heart Failure
  • Coronary arteriography
    • Should be performed in patients presenting with heart failure who have angina or significant ischemia
    • Reasonable in patients who have chest pain that may or may not be cardiac in origin, in whom cardiac anatomy is not known, and in patients with known or suspected coronary artery disease who do not have angina.
    • Measure cardiac output, degree of left ventricular dysfunction, and left ventricular end-diastolic pressure.
further testing in heart failure
Further testing in Heart Failure
  • Endomyocardial biopsy
      • Not frequently used
      • Amyloidosis, giant-cell myocarditis
slide20
Aggravating Factors
  • Medications
  • New heart disease
  • Myocardial ischemia
  • Pregnancy
  • Arrhythmias (AF)
  • Infections
  • Thromboembolism
  • Hyper/hypothyroidism
  • Endocarditis
  • Obesity
  • Hypertension
  • Physical activity
  • Dietary excess
slide21
Heart Failure and Myocardial Ischemia
  • Coronary HD is the cause of 2/3 of HF
  • Segmental wall motion abnormalities are not specific if ischemia
  • Angina coronary angio and revascularization
  • No angina
    • Search for ischemia and viability in all ?
    • Coronary angiography in all ?
slide22
ACE-i. Mechanism of Action

VASOCONSTRICTION

VASODILATATION

ALDOSTERONE

PROSTAGLANDINS

VASOPRESSIN

tPA

Kininogen

SYMPATHETIC

Kallikrein

Angiotensinogen

RENIN

BRADYKININ

Angiotensin I

A.C.E.

Kininase II

Inhibitor

ANGIOTENSIN II

Inactive Fragments

slide23
ACE-I. Clinical Effects
  • Improve symptoms
  • Reduce remodelling / progression
  • Reduce hospitalization
  • Improve survival
slide24
Mortality Reduction with ACE-i

Study ACE-i Clinical Seting

CONSENSUS Enalapril CHF

SOLVD treatment Enalapril CHF

AIRE Ramipril CHF

Vheft-II Enalapril CHF

TRACE Trandolapril CHF / LVD

SAVE Captopril LVD

SMILE Zofenopril High risk

HOPE Ramipril High risk

slide25
ACE-i

0.8

0.7

Placebo

0.6

Probabiilityof

Death

p< 0.001

0.5

0.4

p< 0.002

0.3

Enalapril

0.2

0.1

0

0

1

2

3

4

5

6

7

8

9

10

11

12

CONSENSUS

N Engl J Med 1987;316:1429

Months

slide26
ACE-i

30

Asymptomatic

ventricular

dysfunction post MI

Placebo

n=1116

20

Mortality,

%

Captopril

n=1115

10

n = 2231

3 - 16 days post AMI

EF < 40

12.5 --- 150 mg / day

² -19%

p=0.019

0

SAVE

N Engl J Med 1992;327:669

0

3

4

1

2

Years

slide27
ACE-i. Indications
  • Symptomatic heart failure
  • Asymptomatic ventricular dysfunction

- LVEF < 35 - 40 %

  • Selected high risk subgroups

AHA / ACC HF guidelines 2001

ESC HF guidelines 2001

slide28
ACE-i. Practical Use
  • Start with very low dose
  • Increase dose if well tolerated
  • Renal function & serum K+ after 1-2 w
  • Avoid fluid retention / hypovolemia (diuretic use)
  • Dose NOT determined by symptoms
slide29
ACE-i. Dose (mg)

Initial Maximum

Captopril 6.25 / 8h 50 / 8h

Enalapril 2.5 / 12 h 10 to 20 / 12h

Fosinopril 5 to 10 / day 40 / day

Lisinopril 2.5 to 5.0 / day 20 to 40 / day

Quinapril 10 / 12 h 40 / 12 h

Ramipril 1.25 to 2.5 / day 10 / day

AHA / ACC HF guidelines 2001

slide30
ACE-I. Adverse Effects
  • Hypotension (1st dose effect)
  • Worsening renal function
  • Hyperkalemia
  • Cough
  • Angioedema
  • Rash, ageusia, neutropenia, …
slide31
ACE-I. Contraindications
  • Intolerance (angioedema, anuric renal fail.)
  • Bilateral renal artery stenosis
  • Pregnancy
  • Renal insufficiency (creatinine > 3 mg/dl)
  • Hyperkalemia (> 5,5 mmol/l)
  • Severe hypotension
slide32
ß-Adrenergic Blockers

Mechanism of action

  • Density of ß1 receptors
  • Inhibit cardiotoxicity of catecholamines
  • Neurohormonalactivation
  • HR
  • Antiischemic
  • Antihypertensive
  • Antiarrhythmic
  • Antioxidant, Antiproliferative
slide33
ß-Adrenergic Blockers

100

90

80

Survival

%

Carvedilol

70

p=0.00014

35% RR

60

Placebo

N = 2289

III-IV NYHA

50

0

4

8

12

16

20

24

28

Months

COPERNICUS

NEJM 2001;344:1651

slide34
ß-Adrenergic Blockers

When to start

  • Patient stable
    • No physical evidence of fluid retention
    • No need for i.v. inotropic drugs
  • No contraindications
  • In hospital or not
slide35
ß-Adrenergic Blockers

Dose (mg)

Initial Target

Bisoprolol 1.25 / 24h 10 / 24h

Carvedilol 3.125 / 12h 25 / 12h

Metoprolol succinnate12,5-25 / 24h 200 / 24h

  • Start Low, Increase Slowly
  • Increase the dose every 2 - 4 weeks
slide36
ß-Adrenergic Blockers

Adverse Effects

  • Hypotension
  • Fluid retention / worsening heart failure
  • Fatigue
  • Bradycardia / heart block
slide37
Aldosterone Inhibitors

ALDOSTERONE

Spironolactone

-

Competitive antagonist of the

aldosterone receptor

(myocardium, arterial walls, kidney)

  • Retention Na+
  • Retention H2O
  • Excretion K+
  • Excretion Mg2+
  • Collagen
  • deposition
  • Fibrosis
  • - myocardium
  • - vessels

Edema

Arrhythmias

slide38
1.0

0.9

0.8

0.7

0.6

0.5

0

6

12

24

30

36

18

Spironolactone

Annual Mortality

Aldactone 18%; Placebo 23%

Survival

Aldactone

N = 1663

NYHA III-IV

Mean follow-up 2 y

p < 0.0001

RALES

NEJM 1999;341:709

Placebo

months

slide39
Spironolactone.Indications
  • Recent or current symptoms despite ACE-i, diuretics, dig. and b-blockers
  • AHA / ACC HF guidelines 2001
  • Recommended in advanced heart failure (III-IV), in addition to ACE-i and diuretics
  • Hypokalemia
  • ESC HF guidelines 2001
slide40
Spironolactone.Practical use
  • Do not use if hyperkalemia, renal insuf.
  • Monitor serum K+ at “frequent intervals”
  • Start ACE-i first
  • Start with 25 mg / 24h
  • If K+ >5.5 mmol/L, reduce to 25 mg / 48h
  • If K+ is low or stable consider 50 mg / day
  • New studies in progress
slide41
Angiotensin II Receptor Blockers (ARB)

RENIN

Angiotensin IANGIOTENSIN II

Angiotensinogen

ACE

Other pathways

AT1

Receptor

Blockers

RECEPTORS

AT1

AT2

Vasoconstriction

Proliferative

Action

Vasodilatation

Antiproliferative

Action

slide42
Angiotensin II Receptor Blockers (ARB)
  • Candesartan, Eprosartan, Irbesartan

Losartan, Telmisartan, Valsartan

  • Not indicated with beta blockers
  • Indicated in patients intolerant to ACE-I

AHA / ACC HF guidelines 2001

ESC HF guidelines 2001

slide43
Positive Inotropes
  • Digitalis
  • Sympathomimetics
    • Catecholamines
    • B-adrenergic agonists
  • Phosphodiesterase inhibitors
    • Amrinone, Milrinone, Enoximone
  • Calcium sensitizers
    • Levosimendan, Pimobendan
slide44
Positive Inotropic Therapy
  • May increase mortality

Exception: Digoxin, Levosimendan

  • Use only in refractory CHF
  • NOT for use as chronic therapy
slide45
- PlasmaNoradrenaline

- Peripheral nervous system activity

- RAAS activity

- Vagaltone

- Normalizes arterial baroreceptors

Digitalis. Mechanism of Action

Blocks Na+ / K+ ATPase => Ca+ +

•Inotropic effect

•Natriuresis

•Neurohormonal control

NEJM 1988;318:358

slide46
Digitalis. Clinical Effects
  • Improve symptoms
  • Modest reduction in hospitalization
  • Does not improve survival
slide47
Digitalis. Indications

• When no adequate response to

ACE-i + diuretics + beta-blockers

AHA / ACC Guidelines 2001

• In combination with ACE-i + diuretics

if persisting symptoms

ESC Guidelines 2001

• AF, to slow AV conduction

Dose 0.125 to 0.250 mg / day

slide48
50

40

30

20

10

0

Digitalis

Mortality

%

Placebo

n=3403

p = 0.8

N=6800

NYHA II-III

Digoxin

n=3397

0

12

24

36

48

DIG

N Engl J Med 1997;336:525

Months

slide49
Diuretics. Indications
  • 1. Symptomatic HF, with fluid retention
    • Edema
    • Dyspnea
    • Lung Rales
    • Jugular distension
    • Hepatomegaly
    • Pulmonary edema (Xray)

AHA / ACC HF guidelines 2001

ESC HF guidelines 2001

slide50
Loop Diuretics / Thiazides. Practical Use
  • Start with variable dose. Titrate to achieve dry weight
  • Monitor serum K+ at “frequent intervals”
  • Reduce dose when fluid retention is controlled
  • Teach the patient when, how to change dose
  • Combine to overcome “resistance”
  • Do not use alone
slide51
Thiazides, Loop Diuretics. Adverse Effects

• K+, Mg+ (15 - 60%) (sudden death ???)

• Na+

• Stimulation of neurohormonal activity

• Hyperuricemia (15 - 40%)

• Hypotension. Ototoxicity. Gastrointestinal. Alkalosis. Metabolic

Sharpe N. Heart failure. Martin Dunitz 2000;43

Kubo SH , et al. Am J Cardiol 1987;60:1322

MRFIT, JAMA 1982;248:1465

Pool Wilson. Heart failure. Churchill Livinston 1997;635

slide52
Diuretic Resistance
  • Neurohormonal activation
  • Rebound Na+ uptake after volume loss
  • Hypertrophy of distal nephron
  • Reduced tubular secretion (renal failure, NSAIDs)
  • Decreased renal perfusion (low output)
  • Altered absortion of diuretic
  • Noncompliance with drugs

Brater NEJM 1998;339:387

Kramer et al. Am J Med 1999;106:90

slide53
Managing Resistance to Diuretics

• Restrict Na+/H2O intake (Monitor Natremia)

• Increase dose (individual dose, frequency, i.v.)

• Combine: furosemide + thiazide / spiro / metolazone

• Dopamine (increase cardiac output)

• Reduce dose of ACE-i

• Ultrafiltration

Motwani et al Circulation 1992;86:439

slide54
Drugs to Avoid (may increase symptoms, mortality)
  • Inotropes, long term / intermittent
  • Antiarrhythmics (except amiodarone)
  • Calcium antagonists (except amlodipine)
  • Non-steroidal antiinflammatory drugs (NSAIDS)
  • Tricyclic antidepressants
  • Corticosteroids
  • Lithium

ESC HF guidelines 2001

slide55
Refractory End-Stage HF
  • Review etiology, treatment & aggrav. factors
  • Control fluid retention
    • Resistance to diuretics
    • Ultrafiltration ?
  • iv inotropics / vasodilators during decompensation
  • Consider resynchronization
  • Consider mechanical assist devices
  • Consider heart transplantation
cardiac resynchronization therapy in patients with severe systolic heart failure
Cardiac Resynchronization Therapy* in Patients With Severe Systolic Heart Failure
  • For patients who have left ventricular ejection fraction (LVEF) less than or equal to 35%, a QRS duration greater than or equal to 0.12 seconds, and sinus rhythm, cardiac resynchronization therapy (CRT) with or without an ICD is indicated for the treatment of New York Heart Association (NYHA) functional Class III or ambulatory Class IV heart failure symptoms on optimal recommended medical therapy
slide58
Heart Transplant. Indications
  • Refractory cardiogenic shock
  • Documented dependence on IV inotropic support to maintain adequate organ perfusion
  • Peak VO2 < 10 ml / kg / min
  • Severe symptoms of ischemia not amenable to revascularization
  • Recurrent symptomatic ventricular arrhythmias refractory to all therapeutic modalities

Contraindications: age, severe comorbidity

slide59
Ventricular Arrhythmias / Sudden Death
  • Antiarrhythmics ineffective (may increase mortality)

Amiodarone do not improve survival

  • -blockers reduce all cause mortality and SD
  • Control ischemia
  • Control electrolyte disturbances
  • ICD (Implantable Cardiac Defibrillator)
    • In secondary prevention of SD
    • In sustained, hemodynamic destabilizing VT
    • Ongoing research will establish new indications
slide61
Diastolic Heart Failure
  • Incorrect diagnosis of HF
  • Inaccurate measurement of LVEF
  • Primary valvular disease
  • Restrictive (infiltrative) cardiomyopathies (Amyloidosis…)
  • Pericardial constriction
  • Episodic or reversible LV systolic dysfunction
  • Severe hypertension, ischemia
  • High output states: Anemia, thyrotoxicosis, etc
  • Chronic pulmonary disease with right HF
  • Pulmonary hypertension
  • Atrial myxoma
  • LV Hypertrophy
  • Diastolic dysfunction of uncertain origin
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