Left ventricular (LV) performance (FrankStarling) curves relate preload, measured as LV end-diastolic volume
(EDV) or pressure (EDP), to cardiac performance, measured as ventricular stroke volume or cardiac output.
On the curve of a normal heart (middle line), cardiac performance continuously increases as a function of
preload. States of increased contractility (e.g., norepinephrine infusion) are characterized by an augmented
stroke volume at any level of preload (upper line). Conversely, decreased LV contractility (commonly associated
with heart failure) is characterized by a curve that is shifted downward (lower line). Point a is an example of a
normal person at rest. Point b represents the same person after developing systolic dysfunction and heart
failure (e.g., after a large myocardial infarction): stroke volume has fallen, and the decreased LV emptying
results in elevation of the EDV. Because point b is on the ascending portion of the curve, the elevated EDV
serves a compensatory role because it results in an increase in subsequent stroke volume, albeit much less
than if operating on the normal curve. Further augmentation of LV fi lling (e.g., increased circulating volume) in
the heart failure patient is represented by point c, which resides on the relatively fl at part of the curve: stroke
volume is only slightly augmented, but the signifi cantly increased EDP results in pulmonary congestion.
Afterload the ventricular wall stress ( ) that develops
during systolic ejection.
Systolic Dysfunction
Coronary Artery Disease
Hypertension
Valvular Heart Disease
Diastolic Dysfunction
Hypertension
Coronary artery disease
Hypertrophic obstructive cardiomyopathy
(HCM)
Restrictive cardiomyopathy
EJECTION FRACTION
ReninAngiotensinAldosterone System
The main stimuli for renin secretion from the juxtaglomerular cells of the kidney in heart
failure patients :
1. Decreased renal artery perfusion pressure secondary to low cardiac output,
2. Decreased salt delivery to the macula densa of the kidney owing to alterations in
intrarenal hemo dynamics, and
3. Direct stimulation of juxtaglomerular 2-receptors by the activated adrenergic
nervous system.
Neurohormonal Alterations
Antidiuretic Hormone
Secretion of this hormone (also termed vasopressin) by the posterior pituitary is
increased in many patients with heart failure, presumably mediated through arterial
baroreceptors, and by increased levels of AII. ADH contributes to increased
intravascular volume because it promotes water retention in the distal nephron.
Natriuretic Peptides
Atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP).
They result in excretion of sodium and water, vasodilatation, inhibition of renin
secretion, and antagonism of the effects of AII on aldosterone and vasopressin levels.
COMPENSATORY MECHANISMS
Neurohormonal Alterations
Compensatory neurohormonal
stimulation develops in response to the
reduced forward cardiac output and
blood pressure of heart failure.
ReninAngiotensinAldosterone System
PRECIPITATING FACTORS
HOW HEART FAILURE IS DIAGNOSED
Systolic dysfunction:
Reduced LVEF (<45%)
Thin LV wall
Eccentric LV remodeling
Pulmonary hypertension
Diastolic dysfunction:
Normal LVEF (45%-50%)
Normal LV size
Concentric LV remodeling
Pulmonary hypertension
Upright position
Nitrates
Lasix
Oxygen
ACE inhibitors
Digoxin
Fluids(decrease)
After load (decrease)
Sodium retention
Test (Dig level, ABGs, Potassium level)
THERAPEUTIC ALGORITHM HFREF
Acute Heart Failure
Rapid onset of symptoms and signs secondary to
abnormal cardiac function
Can present as new onset and without previously known
cardiac dysfunction or ADHF
Often life threatening and requires urgent treatment
Pulmonary congestion
ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure
European Heart Journal, 2016
CAUSES AND PRECIPITATING FACTORS
Ischaemic heart disease
Acute coronary syndrome
Mechanical complications of acute MI
RV infarction
Valvular
Valve stenosis
Valvular regurgitation
Endocarditis
Aortic dissection
Myopathies
Postpartum cardiomyopathy
Acute myocarditis
Hypertension/arrhythmias
Circulatory failure
Septicaemia
Thyrotoxicosis
Anaemia
Tamponade
Pulmonary embolism
Decompensation of pre-existing CHF
Volume overload
Infection
Cerebrovascular insult
Surgery
Renal dysfunction
Asthma, COPD
Drug and alcohol abuse
DIAGNOSTIC OF ACUTE HEART FAILURE
Based on presenting symptoms and clinical
findings
History
Physical examination
ECG
Chest X-ray
Echocardiography
Laboratory (BGA, etc)
ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure
European Heart Journal, 2008
FLUID OVERLOAD > Acute Decompensated Heart
Failure (ADHF)/Pulmonary Edema
>Medical Emergency!
MONITORING
Non invasive:
Vital Sign
Oxygenation
Urine output
ECG
Invasive:
Arterial line (haemodynamic unstable)
Central venous lines
Pulmonary artery catheter
Coronary angiography
GOALS OF TREATMENT
Immediate (ED/ICU/ICCU)
Improved symptom
Intermediate (hospital)
Stabilize patient & optimize treatment strategy
Education
Prevention
Quality of life
MANAGEMENT
ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure
European Heart Journal, 2008
OXYGEN
ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure
European Heart Journal, 2008
LOOP DIURETICS
ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure
European Heart Journal, 2008
VASODILATORS
ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure
European Heart Journal, 2008
INOTROPIC AGENTS
ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure
European Heart Journal, 2008
PATIENT COUNSELING
Lifestyle changes
Medications
Surgery
PATIENT COUNSELING
Lifestyle changes
Stop smoking
Loose weight
Avoid or limit alcohol
Avoid or limit caffeine
Eat a low-fat, low-sodium diet
Exercise
PATIENT COUNSELING
Reduce stress
Keep track of symptoms and weight
and report any changes or concern to
the doctor
Limit fluid intake
See the doctor more frequently
HEART FAILURE
COMPLICATIONS
Pleural effusion
Atrial fibrillation (most common
dysrhythmia)
Loss of atrial contraction (kick) -reduce CO by
10% to 20%
Promotes thrombus/embolus formation inc.
risk for stroke
Treatment may include cardioversion,
antidysrhythmics, and/or anticoagulants
HEART FAILURE
COMPLICATIONS
**High risk of fatal dysrhythmias (e.g., sudden
cardiac death, ventricular tachycardia) with HF
and an EF <35%