ACUTE AND CHRONIC HEART FAILURE

SYSTOLIC AND DIASTOLIC HEART FAILURE

Ali Aspar Mappahya

Cardiology Department, Medical Faculty, Hasanuddin University
 INTRODUCTION

Heart failure (HF) is a major health problem, it will be a major

cause of morbidity and mortality in the future.

HF: Cardiac disorders that impairs the capacity of the

ventricle to fill or to eject the appropriate amount of blood.

HF: The inability of the heart to perfuse metabolizing tissues

adequately.
 INTRODUCTION.

The risk factors for HF among HTN subjects included

MCI (5-6 fold risk), LVH (2-3 fold risk), DM (2-3 fold risk)
and valvular heart disease ( two-fold risk).

In developed countries, there are two principal risk factors

for HF : hypertension (HTN) and myocardial infarction
(MCI)

Early and adequate treatment of HTN may substantially

reduce the burden of heart failure in the community.

Despite these treatments, morbidity and mortality

remain high.
 DEFINITION OF HEART FAILURE (HF)
HF is a clinical syndrome in which patients
have the following features :
Symptoms typical of HF :
(breathlessness at rest or on exercise, fatigue, tiredness,
ankle swelling).

Signs typical of HF :
(tachycardia, tachypnea, pulmonary rales, pleural effusion,
raised jugular venous pressure, peripheral edema,
hepatomegaly).

Objective evidence of a structural or functional abnormality

of the heart at rest :
(cardiomegaly, S3, cardiac murmur, abnormality on the
echocardiogram, raised natriuretic peptide concentration).
 PREDISPOSING CAUSES OF HEART FAILURE

Hypertension
Diabetes Mellitus Alcohol abuse
Dyslipidemia Smoking
Valvular heart disease Collagen vascular
Coronary artery disease disease
Myopathy Thyroid disorder
Rheumatic fever Pheochromocytoma
Mediastinal radiation Old age
Sleep apnea disorders Metabolic syndrome
Exposure to cardiotoxin
agents
 PRECIPITATING FACTORS OF HEART FAILURE

1. Infections
2. Brady-or tachyarrhythmia
3. Myocardial ischemia or infarction (MI)
4. Physical or emotional stress
5. Pulmonary embolism
6. High-output states such anemia, thyrotoxicosis, Pagets
disease, pregnancy, beriberi and A-V fistula
7. Cardiac infection and inflammation (myocarditis, infective
endocarditis)
8. Comorbidities (renal, liver, thyroid, respiratory
insufficiency)
9. Cardiac toxin (chemotherapy, cocain, alcohol etc)
Relationship between end-diastolic volume and stroke
volume in normal and failing myocardium
Pathophysiology of Heart Failure
 Chronic Heart Failure

Systolic Failure Diastolic Failure

 Pathophysiology of Systolic Heart Failure
Neurohormonal Activation and Imbalance

Vasodilating and
growth inhibiting
Vasoconstricting and Natriuretic peptides
growth promoting Bradykinin
Norepinephrine Nitric oxide/EDHF
Angiotensin II Prostaglandins
Endothelins
Arginine vasopressin Improve hemodynamics,
prevent remodeling
Worsen hemodynamics,
progressive remodeling

Anand IS, Chugh SS. Curr Opin Cardiol. 1997;12:251-258.

 Neurohormonal Activation in Heart Failure

Plasma Plasma renin Arginine Atrial natriuretic

norepinephrine activity vasopressin peptide Endothelin-1
(pg/mL) (ng/mL/h) (pg/mL) (pg/mL) (pg/mL)

600 15 12 300 8

500 250
12
6 6
400 200
Levels

9
300 4 150 4
6
200 100
2 2
100 3 50

0 0 0 0 0
NL HF NL HF NL HF NL HF NL HF

Cohn 1997.
 Obesity
Diabetes
LVH
Diastolic
Dysfunction
Hypertension
CHF Death

Systolic
MI Dysfunction
Smoking
Dyslipidemia
Diabetes

Normal LV LV Subclinical
Overt HF
structure and function remodelling LV dysfunction

Time (decades) Time (months)

The progression from hypertension to CHF

 NYHA Functional Classification of HF
Severity based on symptoms and physical activity

Class I No limitation of physical activity. Ordinary physical

activity does not cause undue fatigue, palpitation or
dyspnea.
Class II Slight limitation of physical activity. Comfortable at rest,
but ordinary physical activity results in fatigue,
palpitation, or dyspnea.
Class III Marked limitation of physical activity. Comfortable at
rest, but less than ordinary activity results in fatigue,
palpitation or dyspnea.
Class IV Unable to carry on any physical activity without
discomfort. Symptoms at rest. If any physical activity is
undertaken, discomfort is increased.
 ACC/AHA Stages of HF
Based on structure and damage to heart muscle

Stage A At high risk for developing HF. No identified

structural or functional abnormality; No signs or
symptoms.
Stage B Developed structural heart disease that is strongly
associated with the development of HF, but
without signs or symptoms.
Stage C Symptomatic HF associated with underlying
structural heart disease.

Stage D Advanced structural heart disease and marked

symptoms of HF at rest despite maximal medical
therapy.
 ACC / AHA Classification of CHF2001
STAGE DESCRIPTION

A
High Risk For Hypertension, Diabetes Mellitus, CAD,
Developing Heart Family History of Cardiomyopathy
Failure

B Previous MI, LV Dysfunction,

Asymptomatic
Valvular Heart Disease
Heart Failure

C Structural Heart Disease, Dyspnea and

Symptomatic Fatigue, Impaired Exercise Tolerance
Heart Failure

D Marked Symptoms at Rest Despite

Refractory End-stage Maximal Medical Therapy
Heart Failure
FORWARD
EFFECTS

Poor renal perfusion predisposing to

prerenal failure.

Poor perfusion of extremities resulting in

cold extremities.

Increased lactic acid production in under-

perfused skeletal muscle leading to
weakness and fatigue.

Hypotension
BACKWARD
EFFECTS

The peripheries subcutaneous edema is

felt in the legs and other dependents part.

The liver tender hepatomegaly is a result

of hepatic congestion and may lead to
cirrhotic changes.

The abdominal cavity resulting in ascites

 COMMON CLINICAL MANIFESTATIONS OF HF
Dominant Symptoms Signs
clinical feature
Peripheral edema/ Breathlessness, tiredness, Peripheral edema, raised JVP,
congestion fatigue, anorexia pulmonary edema,
hepatomegaly, ascites, fluid
overload, cachexia
Pulmonary edema Severe brathlessness at Crackles or rales over lungs,
rest effusion, tachycardia, tachypnea
Cardiogenic shock Confusion, weakness, Poor peripheral perfusion,
(LOS) cold periphery systolic BP <90 mmHg, anuria
or oliguria
High BP Breathlessness Usually raised BP, LVH, and
(Hypertensive HF) preserved EF
Right heart failure Breathlessness, fatigue Evidence of RV dysfunction,
raised JVP, peripheral edema,
hepatomegaly, gut congestion
 CONDITIONS ASSOCIATED WITH
A POOR PROGNOSIS IN HF

1. DEMOGRAPHICS: 2. CLINICAL:
- Advanced aged* - Hypotension*
- Ischemic etiology* - NYHA class III_IV*
- Resuscitated- - Recent HF-
sudden death* hospitalization*
- Poor compliance - Tachycardia
- Renal dysfunction - Pulmonary rales
- Diabetes - Aortic stenosis
- Anemia - Low BMI
- COPD - Sleep related
- Depression breathing disorders
* = powerful predictors
 CONDITIONS ASSOCIATED

3. ELECTROPHYSIOLOGICAL:
- Tachycardia 4. FUNCTIONAL/
- Q-waves EXERTIONAL:
- Wide QRS* - Reduced work
- LVH - Low peak VO2*
- Complex ventricular- - Poor 6 minutes-
arrhythmias* walk distance
- Low HR variability - High VE/VCO2-
- T-wave alternans slope
- Atrial fibrillation (AF) - Periodic breathing

* = powerful predictors
 CONDITIONS ASSOCIATED
5. LABORATORY:
- Marked elevation of BNP/
NT-pro BNP*
- Hyponatremia*
- Elevated troponin*
- Elevated biomarkers,
neurohumoral activation*
- Elevated creatinine/
BUN
- Elevated bilirubin
- Anemia
- Elevated uric acid
* = powerful predictors
6. IMAGING:
- Low LVEF*
- Increased LV vol.
- Low cardiac index
- High LV filling-
pressure
- Restrictive mitral-
filling pattern
- Pulmonary htn.
- Impaired RV -
function
 EVOLUTION OF CLINICAL
STAGES

NORMAL
No symptoms Asymptomatic LV
Normal exercise
Normal LV fxn Dysfunction
No symptoms Compensated
Normal exercise
Abnormal LV fxn CHF
No symptoms Decompensated
Exercise
Abnormal LV fxn
CHF
Symptoms Refractory
Exercise
Abnormal LV fxn
CHF
Symptoms not
controlled with
treatment
 MAIN STRATEGIES FOR PATIENTS WITH
CHRONIC CONGESTIVE HEART FAILURE

1. Life style modification.

2. Prevent precipitating and aggravating factors.
3. Essential pharmacologic management with BB, ACEI/ARB.
4. Complimentary treatment with diuretics or vasodilators.
5. Reverse structural abnormalities (remodeling with
hypertrophy or dilation).
6. Device therapy including implantable cardioverter
defibrillation (ICD), bi-ventricular pacing.
 Stages in the evolution of HF and recommended therapy by stage

Stage A Stage B Stage C Stage D

Pts with : Pts with : Pts with :

Pts who have marked
Hypertension Previous MI Struct. HD symptoms at rest
CAD LV systolic Refract. despite maximal
Struct. Develop Shortness of breath
DM dysfunction medical therapy.
Cardiotoxins Heart Asymptomatic Symp.of and fatigue, reduce Symp.of
exercise tolerance
FHx CM Disease Valvular disease HF HF at rest

THERAPY THERAPY THERAPY THERAPY

Treat Hypertension All measures under All measures under All measures under
Stop smoking stage A stage A stage A,B and C
Treat lipid disorders ACE inhibitor Drugs for routine use: Mechanical assist
Encourage regular Beta-blockers diuretic device
exercise ACE inhibitor Heart transplantation
Stop alcohol Beta-blockers Continuous IV
& drug use digitalis inotrphic infusions for
ACE inhibition palliation

ACC/AHA Guidelines for the

Evaluation and Management of Chronic Heart Failure in the Adult 2001
 PHARMACOLOGIC MANAGEMENT OF PATIENTS
WITH HF AND CORONARY ARTERY DISEASE (CAD)

ACEIs : are recommended in CAD with impaired LVEF (40%).

ARBs : are recommended in patients following MCI with symptoms of

HF or impaired LVEF intolerant to ACEI.

BBs : are recommended for CAD patients with symptoms of HF and

impaired LVEF.
Aldosterone antagonists: are recommended in patients following MCI with
impaired LVEF and/or signs and symptoms of HF.

Nitrates: may be considered to control anginal symptoms.

CCB : may be considered to control anginal symptoms in patients with
reduced LVEF, amlodipine or felodipine are preferable.

Statins: may be considered for all patients with HF and CAD.

No evidence improve survival, but may be reduce the risk of hospitalization.
 MANAGEMENT OF PATIENTS WITH HF AND
PRESERVED LVEF (HFPEF)
DIASTOLIC HF

No treatment has yet been shown, convincingly, to reduce

morbidity and mortality in patients with HFPEF.

Diuretics are used to control sodium and water retention

and relieve breathlessness and edema.

Adequate treatment of hypertension and myocardial

ischemia is also important, as is control of the
ventricular rate.

We can use ACEI or ARB

 ARRHYTHMIAS IN HF

ATRIAL FIBRILLATION (AF)

A beta-blocker (BB) or digoxin is recommended to control the heart
rate at rest in patient with HF and LV dysfunction.

A combination of digoxin and BB may be considered to control heart

rate at rest and during exercise.

In LV systolic dysfunction, digoxin is the recommended initial

treatment if the patient is hemodynamically unstable.

Intravenous administration of digoxin or amiodarone is recommended

to control the heart rate in patient with AF and HF,
who do not have an accessory pathway.
 Prevention of thromboembolism :
Antithrombotic therapy to prevent thromboembolism is recommended
to all patients with AF, unless contra-indicated.

In patients with AF at highest risk of stroke/thromboembolism, chronic

oral anticoagulant therapy with a vitamin K antagonist
is recommended unless contra-indicated.

Rhythm control :
Electrical cardioversion is recommended when the rapid ventricular
response does not respond promptly to appropriate pharmacological
measures, especially in patients with AF causing myocardial ishemia,
symptomatic hypotension or symptom of pulmonary congestion.
 VENTRICULAR ARRHYTHMIAS (VA)
It is essential to detect, and if possible, correct all potential factors
precipitating ventricular arrhythmias. Neurohumoral blockade with
optimal doses of BB, ACEI, ARB and/or aldosterone blockers is
recommended.

Routine prophylactic use of antiarrhythmic agents in patients with

asymptomatic, non sustained VA is not recommended.
In HF patients, Class Ic agents should not be used
 Patients with HF and symptomatic VA :

In patients who survived VF or had a history of hemodynamically

unstable Ventricular tachycardia (VT) or VT with syncope, with reduced
LVEF (< 40%), receiving optimal pharmacological treatment and with
a life expectancy of > 1 year, ICD implantation is recommended.

Amiodarone is recommended in patients with an implanted ICD,

otherwise optimal treated, who continue to have symptomatic VA.

Catheter ablation is recommended as adjunct therapy in patients with

ICD implanted who have recurrent symptomatic VT.
 MANAGEMENT OF ARTERIAL HYPERTENSION IN HF

In hypertensive patients with evidence of LV dysfunction :

Systolic and diastolic BP should be carefully controlled with a
therapeutic target of 140/90 and 130/80 mmHg in diabetics and
high risk patients.

Anti-hypertensive regimens based on renin-angiotensin system antagonists

(ACEI or ARBs) are preferable.

In hypertensive patients with HFPEF :

Aggressive treatment (often with several drugs with complementary

mechanisms of action) is recommended.

ACEI and/or ARBs should be considered the first-line agents.

 RENAL DYSFUNCTION IN HF

Renal dysfunction is common in HF and the prevalence

increases with HF severity, age, a history of HTN or DM

In HF renal dysfunction is strongly linked to increased

morbidity and mortality.

The cause of renal dysfunction should always be sought

in order to detect potentially reversible causes such as
hypotension, dehydration, deterioration in renal function
due to ACEI, ARBs or other concomitant medications
(e.g. NSAIDs) and renal artery stenosis.
 CHRONIC OBSTRUCTIVE PULMONARY DISEASE IN HF

COPD is a frequent comorbidity in HF. Restrictive and obstructive

pulmonary abnormalities are common.

There are significant overlap in the signs and symptoms with a relatively
lower sensitivity of diagnostic tests such as Chest X-ray, ECG,
echocardiography and spirometry.
It is essential to detect and treat pulmonary congestion.
Agents with documented effect on morbidity and mortality sych as ACEI,
BB and ARBs are recommended in patients with co-existing pulmonary
disease.

The majority of patients with HF and COPD can safely tolerate BB

therapy. Mild deterioration in pulmonary function and symptoms should
not lead to prompt discontinuation.

A history of asthma should be considered a contraindication to use BB.

 ACUTE HEART FAILURE (AHF)
DEFINITION :

AHF is defined as a rapid onset or change in the signs

and symptoms of HF, resulting in the need of urgent
therapy.

It may present as new HF or worsening HF in the presence

of chronic HF.

It may be associated with worsening symptoms or signs or

as a medical emergency such as
Acute Pulmonary Edema.
The patients with AHF will usually present
in one of 6 clinical categories

1. Worsening or decompensated Chronic HF :

2. Acute pulmonary edema.
3. Hypertensive HF.
4. Cardiogenic shock.
5. Isolated right HF.
6. Acute Coronary Syndrome and HF
 CAUSES AND PRECIPITATING FACTORS OF AHF

ACS, Mechanical complications of AMI, RV Infarction.

Valve stenosis, Valvular regurgitation, Endocarditis, Aortic dissection.

Postpartum cardiomyopathy, Acute myocarditis.

Hypertension, Acute arrhythmias.

Septicemia, Thyrotoxicosis, Anemia, Shunts, Tamponade, Pulmonary

embolism.

Decompensation of preexisting Chronic HF:

Volume overload, Infections (pneumonia), Cerebrovascular insult,
Surgery, Renal dysfunction, Asthma, Drug abuse, Alcohol abuse.
 GOALS OF TREATMENT IN AHF
Immediate (ED/ICU/CCU):
Improve symptoms
Restore oxygenation
Improve organ perfusion and hemodynamic
Limit cardiac/renal damage
Minimize ICU length of stay

Intermediate (In hospital):

Stabilize patients and optimize treatment strategy
Initiate appropriate (life-saving) pharmacological therapy
Consider device therapy in appropriate patients
Minimize hospital length of stay

Long-term and predischarge management:

Plan follow-up strategy
Educate and initiate appropriate lifestyle adjustments
Provide adequate secondary prophylaxis
Prevent early readmission
Improve quality of life and survival
 The following management options are considered
Appropriate in patients with AHF

o Oxygen : it is recommended to administer O2 as early as possible

in hypoxemic patients to achieve an arterial O2 saturation 95%.

o Non-invasive ventilation (NIV) : (with a sealed face-mask)

NIV with positive end-expiratory pressure (PEEP) should be considered
as early as possible in every patients with Acute cardiogenic pulmonary
edema and hypertensive acute HF.

o Morphine and its analogues in AHF : Morphine relieves dyspnea and

other symptoms in patients with AHF and may be improve cooperation
for the application of NIV (dose: 2,5-5 mg IV line).

o Loop diuretics : Excessive treatment may lead to hypovolemia and

hyponatremia.
 The following management options
o Vasodilators : Are recommended at an early stage for HF patients
without symptomatic hypotension .
Vasodilators relieve pulmonary congestion usually without compromising
stroke volume or increasing oxygen demand in AHF, particularly in
patients with ACS.
Hypotension (SBP <90 mmHg) should be avoided, especially in patients
with renal dysfunction

o Inotropic agents : should be considered in patients with low output state,

in the presence of signs of hypoperfusion or congestion despite the use of
vaso dilators and/or diuretics.
Dopamine, Dobutamine, Milrinone, Enoximone, Levosimendan.

o Vasopressors : Norepinephrine are not recommended as first-line agent

and are only indicated in cardiogenic shock when the combination of an
inotropic agent and fluid challenge fails to restore adequate BP.

o Cardiac glycoside: In AHF, cardiac glycoside produce a small increase

in cardiac output and reduction of filling pressure . It may be useful to
slow ventricular rate in rapid AF