Heart failure

Heart failure is the pathological process in which the heart can’t pump enough blood to meet the metabolic requirements of the body due to impaired systolic or/and diastolic function of the heart.

Blood returning to the heart faster than the heart can eject it congests the system behind it.

Congestive heart failure

Classification

Right, left, whole

Acute, chronic

Low-output, high-output

Systolic, diastolic

Hyperthyroidism

Severe anemia

VitB1 deficiency

Arteriovenous fistula

Etiology

Underling causes

Precipitating factors

Underling causes

Primary systolic and diastolic dysfunction

Excess work demands

Myocardial impairment

myocarditis, cardiomyopathy, myocardial angina, myocardial infarction

Metabolic abnormalities

ischemia, hypoxia, deficiency of VitB1

Primary systolic and diastolic dysfunction

Excess work demands

Pressure overload ( postload )

systemic hypertension, pulmonary hypertension, aortic stenosis, pulmonary embolism

Volume overload (preload)

arteriovenous shunt, thyrotoxicosis, chronic anemia, valvular (mitral, aortic, etc.) regurgitation

Precipitating factors

pulmonary and systemic infection

arrhythmia

Pregnancy and delivery

water-electrolyte and acid-base disturbance

Persistent application of some drugs

others

Compensation and adaptation

Pump reserve

Ventricular remodeling

Neuro-humoral mechanism

Peripheral adaptation Similar to hypoxia

Pump reserve

Frank-Starling mechanism

preload↑→ SV ↑

Myocardial contractility ↑ SN ↑ positive inotropic action

Heart rate ↑ SN ↑

Excessive preload may lead to

Venous congestion↑

Myocardial O2 consumption↑

Coronary perfusion ↓

Myocardial O2 consumption↑

Coronary perfusion ↓

CO↓

Increased preload may be causes by

water and sodium retension

Increased blood back to heart

Decreased stroke volume

Ventricular remodeling

Myocytes hypertrophy, Myocardial hypertrophy

Alteration of myocyte phenotype

Nonmyocyte proliferation, extracellular matrix( ECM) remodeling

Myocardial hypertrophy

Concentric hypertrophy

When the primary stimulus for hypertrophy is pressure overload, the increase in wall stress leads to paralell replication of myofibrils, thickening of the individual myocytes, and concentric hypertrophy.

Eccentric hypertrophy

When the primary stimulus for hypertrophy is volume overload, increased diastolic wall stress leads to replication of myofibrils in series, elongation of the individual myocytes, and concentric hypertrophy.

Alterations of phenotype

Alteration of protein expression

Epigenetic change

Gene mutation

Nonmyocyte proliferation, extracellular matrix( ECM) remodeling

Fibroblast

Macrophage

Endothelia

BV SMC

Collagen Ⅲ

Collagen Ⅰ

Neuro-humoral system

SN-CA

HR ↑,Myocardial contractility ↑

Diverting blood to more critical cerebral and coronary circulations

RAS ↑Ang - vasoconstriction Ⅱ

Aldosterone and ADH salt and water retension

positive

negative

An increase in systemic vascular resistance and the afterload

Decreased blood flow to skin, skeletal muscle, kidney, andominal organs.

Promoting arrhythmia

Increased production of active oxygen species

Exhausting myocardial stores of NE and leading to downregulation and a reduction in β-adrenergic receptors

ANP

Decreased myocardial contractility

Diastolic dysfunction

Pathogenesis

•Myocyte loss and structural change

•Dysfunction of energy metabolism

•Dysfunction of excitation-contraction coupling

mechanism

Decreased myocardial contractility

Myocyte loss and structural change

Necrosis

Hypoxia ,ischemia

Myocardial fibrosis

Toxicity of some humoral factors

Apoptosis

Mitochondria injury

Oxidative stress

Calcium dyshomeostasis

TNF-α

Dysfunction of energy metabolism

Energy production ↓ Ischemia, hypoxia

Mitochondria dysfunction

Energy reserve (CP)↓ CPK(B) ↑, CPK(M) ↓

Energy utilization ↓ Activity of myosin ATPase ↓

V1 ↓, V3 ↑

Dysfunction of excitation-contraction coupling

Reduced Ca 2+ uptake, store and release by SR RyR↓

Reduced influx of extracellular Ca 2+

Dysfunction of Ca2+ binding to troponin

Diastolic dysfunction

Delayed reposition of Ca2+

ATP deficiency

Impaired dissociation of actin-myosin complex

Reduced myocardial compliance↓

hypertrophy, fibrosis, etc

Clinical manifestations

Congestion of pulmonary circulation

Congestion of systemic circulation

Low cardiac output

Congestion of pulmonary circulation

Dyspnea

exertional dyspnea dyspnea related to an increase in activity.

orthopnea shortness of breath that occurs when a person is in supine.

paroxysmal nocturnal dyspnea a sudden attack of dyspnea that occurs during sleep and is precipitated by the development of interstitial pulmonary edema.

Pulmonary edema

Congestion of systemic circulation

Systemic venous congestion and hypertension

Edema

Hepatomegaly and hepatic dysfunction

Low cardiac output

Fatigue, limb weakness, mental confusion, disturbed behavior, cyanosis, reduced urine, cardiac shock

CO 3.5~5.5L/min

CI 2.5~3.5L/min.m-2

EF SV/VEDV 0.56~0.78

VEDV ventricular end diastolic volume

VEDP ventricular end diastolic pressure

PCWP pulmonary capillary wedge pressure 6~12mmHg

CVP central venous pressure 4~12cmH2O

Principle of treatment

General treatment

Improving cardiac function isotropic drugs

Reducing preload and afterload

arterial or venous vasodilators

Controlling edema

restriction of salt intake, diuretics