Date post: | 27-Dec-2015 |
Category: |
Documents |
Upload: | benedict-alexander |
View: | 216 times |
Download: | 2 times |
Chapter 13
Cardiac insufficiency
Introduction
The heart, by virtue of contractile activity of its muscular walls, propels blood throughout the body so as to deliver nutrients to and remove wastes from each of organs. The heart also provides for the transport of hormones and other regulatory substances between various regions of the body. The function of heart as a pump interposed between two interlocking circuits. The overall function of the circulation depends on the satisfactory performance of both cardiac muscle and heart valves. Severe dysfunction of the myocardium may lead to heart failure.
Concept
Heart failure may be defined as the pathological process or syndrome which absolute or relative decrease of cardiac output, namely, to weaken the function of heart pump, by dysfunction of myocardial systole and/or diastole under action of various etiological factors results in being no longer able to meet the metabolic needs of body tissues.
Congestive heart failure usually has a chronic course with an abnormal accumulation of fluid, which results in increase of blood volume, congestion of vein, increase of interstitial fluid and presents edema obviously in clinic.
Myocardial failure refers to the heart failure which is caused by primary dysfunction of myocardial systole and/or diastole.
Heart failure is not a disease; it is a consequence of diseases that impair the ability of heart to function as a pump. Heart failure is a clinical syndrome that may result from a wide spectrum of diseases.
The relationship between heart failure and cardiac insufficiency:
Heart failure belongs to decompensatory phase of CI and cardiac insufficiency includes all courses from complete compensatory to decompesatory phase of the heart. There is no intrinsical difference between them.
Section 1
Etiological causes, Predisposing causes
and Classification of HF
1.1, Etiological Causes
1, Primary dysfunction of myocardial systole and diastole
1) Myocardial damage
For example, Myocarditis, Cardiomyopathies, Myocardial infarction
2) Myocardial ischemia and hypoxia
For example, Coronary heart diseases, Anemia, Hypotension, etc..
2, Overload for myocardium
1) Pressure overload or Excess of after load
For example, Hypertension, aortic stenosis----Pressure overload of left ventricle; Pulmonary hypertension, Pulmonary stenosis, pulmonary embolism, COPD, etc.----- Pressure overload of right ventricle
2) Volume overload or Excess of preload
For example, Mitral and aortic regurgitation for left ventricle; Tricuspid and pulmonary incompetence for right ventricle
1.2, Predisposing causes
90 of patients in HF have predisposing causes. The common predisposing causes i﹪nclude:
1, Infection-----Specially infection of superior respiratory tract is the most common PC.
Mechanism of predisposing HF
1) Fever excitation of sympathetic nerve increase rate of metabolism
enlargement of heart load
2) Endotoxin can directly despress myocardial systole
3) Tachycardia induces increase of oxygen consumption and ischemia and hypoxia in myocardium.
4) The infection of respiratory tract increases heart load and influences supplement of blood and oxgen.
2, Disturbance of acid-base balance and electrolyte metabolism
1) Acidosis
2) Hyperkalemia
a) H+ inhibtes Ca2+ to combine with troponin, internal flow of Ca2+ and decreases Ca2+ release from SR
b) H+ restrains activity of ATP enzyme of myosin
c) H+ induces relaxation of precapillary sphincter and declines blood volume returned to heart and then reduces cardiac output.
a) Hyperkalemia and acidosis depress internal flow of Ca2+ in repolarization and then decline contractibility of myocardium
b) Hyperkalemia results in decrease of myocardial conductibility and then take places arrhythmia
3, Arrhythmia-----especially tachycardia
4, Pregnancy and delivery
a) Tachycardia conduces to shortening of relaxing period of heart and blood supplement of coronary artery declines
b) Tachycardia induces to increase oxygen consumption of myocardium
c) Tachycardia leads to lack of perfusion of heart ventricle and decrease of cardiac output
Increase of blood volume in the stage of pregnancy
Excess of preloada)
b)
Exitation of sympathetico-adrenomedullary system because of pain, anxiety
Increase of backflow of vein Excess of preload
Vasoconstriction of peripheral vessels and increase of resistance
Excess of after load
1.3, Classification 1, According to the time of development
1) Acute heart failure----developed from hours to days, and no enough time for compensatory mechanisms. E.g. acute myocardial infarction, severe myocarditis etc..
2) Chronic heart failure---- developed from weeks to months or years, and fully compensatory mechanisms developed. E.g. hypertension, multivalvular heart diseases, cor pulmonale, etc..
2, According to the cardiac output1) Low output heart failure----caused by hypertension, ischemic heart failure, valvular heart disease and myocarditis. The cardiac output is lower than usuall normal output.
2) High output heart failure---- caused by anemia, beriberi(severe lack of Vit B1), arterio-venous shunting, hyperthyroidism, pregnancy, etc.. The cardiac output is greater than normal but lower than the output before failure.
3, According to the side of disorder
1) Left heart failure----causing obstruction to systemic blood flow, and producing overfilling of pulmonary veins. E.g. coronary heart disease, myocardiopathy, hypertension and mitral incompetence, etc..
2) Right heart failure----causing obstruction to pulmonary blood flow, and producing overfilling of systemic veins. E.g. pulmonary embolism, Pulmonary hypertension, COPD, mitral stenosis, etc..
3) Whole heart failure----right and left sides both are of failure. E.g. rheumatic myocarditis and severe anemia, etc..
4, According to disturbance of systole and diastole of myocardium
1) Heart failure of insufficiency of myocardial systole----e.g. hypertensive heart disease, coronary heart disease, etc..
2) Heart failure of insufficiency of myocardial diastole----e.g. mitral and tricuspid stenosis, constrictive pericarditis, hypertrophic myocardiopathy, etc..
Section 2
Compensation of body in HF
Grade of cardiac compensation;
1) Complete compensation
2) Incomplete compensation
3) decompensation
The cardiac output by compensatory reaction of body suffice a need of normal work and life. The clinical manifestation of HF cannot occur provisionally.
The cardiac output by compensatory reaction of body only suffice a need of body under tranquil and resting condition. The patients have shown mild degree of HF.
The cardiac output by compensatory reaction of body cannot suffice a need of body under tranquil and resting condition. The patients have shown obvious symptoms and sign of HF.
Heart failure
Cardiac insufficiency
2.1, Compensation of heart
1, Increased heart rate
It is a rapid compensatory reaction for elevation of cardiac output, but it is not economical.
Compensatory mechanism include;
1) Role of pressure receptor in carotid sinus and aortic arch
2) Effect of volume receptor in atrium and vena cava
3) Function of chemical receptor in carotid body and aortic body
Limitation –i.e. to be not economical;
1) Increased heart rate results in high oxygen consumption.
2) Heart rate of more than 180 per minute can induce inadequate perfusion of coronary artery and filling of ventricle.
2, Cardiac dilation
It is an important mechanism of regulation for acute hemodynamic change, and as well as called heterometric autoregulation. It conform to law of Frank-Starling.
Initial length of sarcomere
Ten
sion
of
sarc
omer
e
2.2μm 3.65 μm1.7 μm2.1μm
Relation between initial length and tension development in cardiac muscle
There are two kinds of cardiac dilation in HF.
1) Tonic cardiac dilation refers to cardiac relaxation with increase of myocardial contraction. It is compensatory.
2) Myogenic cardiac dilation refers to cardiac relaxation without increase of myocardial contraction. It is decompensatory.
3, Myocardial hypertrophy----long-term adaptation to increased myocardial work
Myocardial hypertrophy refers to aggrandizement of cubage and increase weight in myocardial cell. Exceeding critical value(heart weight more than 500g, or weight of left ventricle more than 200g) induces increase in number of myocardial cell.
Myocardial hypertrophy is divided into two types
1) Concentric hypertrophy
2) Eccentric hypertrophy
Hypertension etc. Increase of Pressure load
Parallel hyperplasia of sarcomere
Increase of thickness of ventricular wall
Without cardiac chamber dilation
Aortic incompetence etc..
Increase of volume load
series hyperplasia of sarcomere
Increase of length of myocardial fiber
With cardiac chamber dilation
Significance of hypertrophy
1) Increased myocardial contraction
2) Decreased tension of ventricular wall and myocardial oxygen consumption
According to Laplace law;
T =p×r
2h
T---Tension of ventricular wall
P--- Pressure within ventricular chamber
R---Semidiameter of cardiac chamber
H---Thickness of ventricular wall
2.2, Compensatory reaction outside heart
1, Increase of blood volume
1) Decreased GFR(glomerular filtration rate)
HF Decreased cardiac output
Decline of arterial pressure
Excitation of sympathetico-adrenomedullary system
Vasoconstriction of renal vessels
Activation of renin-angiotensin-aldosterone system, RAAS
Reduced blood volume in kidney
Fall of synthesization and release of PGE2
2) Increased reabsorption of water and natrium ion in renal tubule
(1) Redistribution of blood flow within kidney
(2) Increased glomerular filtration fraction(FF)
(3) Increased hormones promoting reabsorption of water and natrium ion
For example enhanced renin-angiotensin-aldosterone system, RAAS
(4) Decreased hormones inhibiting reabsorption of water and natrium ion
For example reduced PGE2 and ANP
2, Redistribution of blood flow
3, Increase of red blood cells
4, Increased ability of oxygen utilization in tissue cells
2.3, Adverse influence of long-term compensatory reaction on body
1, Increased pressure load and volume load of heart
2, Increased oxygen consumption
3, Arrhythmia
4, Role of injury of cytokines
5, Oxidative stress
6, Myocardial remodelling
7, Retention of sodium and water
Section 3
Pathogenesis of Heart Failure
肌节中粗细肌丝的组成
3.1, Normal courses of myocardial contraction
肌丝滑行过程
Pathogenesis of Heart Failure
Depressed myocardial contractility
Abnormality of ventricular diastole
Disharmony in contraction and relaxation of heart
3.2, Depressed myocardial contractility
1, Damage of contractive proteins of myocardium
1) Necrosis of myocardial cells----caused by ischemia and hypoxia, bacteria, virus, poisoning(antimony锑 , adriamycin阿霉素 ) , etc..
2) Apoptosis of myocardial cells----caused by
(1) Oxidative stress
(2) Cytokines
(3) Imbalance of homeostasis of Ca2+
(4) Abnormality of mitochondrial function
The most common factor is the acute myocardial infarction.
2, Disorder of energy metabolism of myocardium
1) Disorder in production of energy
2) Disorder in utilization of energy
The most common factor is myocardial ischemia and hypoxia, e.g. ischemic heart diseases, severe anemia, myocardial hypertrophy, lack of VitB1etc..
The most common cause is myocardial hypertrophy in which activity of ATP enzyme in myosin declines
The causes decreased activity of ATP enzyme in myosin are alteration of the structure of peptide chain of ATP enzyme from high active V1(consisting of a couple of -peptide chain) to low active V3 (a couple of -peptide chain)
3, Dysfunction of excitation-contraction coupling
1) Disorder of disposal of Ca2+ in sarcoplasmic reticulum(SR)
(1) Weakened uptake of Ca2+ by SR
HF
Ischemia and hypoxia of myocardium
Decrease of ATP and Ca2+ pump ATPase
Decrease of noradrenalin in myocardium and down-regulation of β-receptor
Weakened uptake of Ca2+ by SR
Bated phosphorylation of PLN
PLN(phospholamban) is a protein of low molecular weight in myocardium, smooth muscle and skeletal muscle. PLN of non-phosphorylation has an inhibition for Ca2+ pump in SR and PLN of phosphorylation can make activity of Ca2+ pump increased.
(2) Reduced reserve of Ca2+ in SR----caused by
(3) Declined release of Ca2+ in SR
a) Weakened uptake of Ca2+ by SR
b) Increased uptake of Ca2+ by mitochondrion
Reduced reserve of Ca2+ in SR
Decreased RyR protein in SR and RyRmRNA
Acidosis to enhance affinity between Ca2+ and calcium store protein in SR
HFDeclined release of Ca2+ in SR
Normal
HF
2) Disorder of Ca2+ inward flow from outside of myocardial cells
There are two paths of Ca2+ inward flow in the myocardial cells. They are channel of Ca2+ inward flow and Na+- Ca2+ exchange.
(1) Ca2+ channel----it included two kinds of channels
a) Voltage-dependent calcium channel(VDC)
b) Receptor-operated calcium channel(ROC)
It is adjusted by membrane potential. When potential within membrane is positive in depolarization VDC opens and Ca2+ outside cells enter into the cytoplasm along the concentration degree. When potential within membrane is negative in repolarization VDC closes up and stops inward flow of Ca2+.
It is controled by β-receptor on the cellular membrane and some of hormones. When NE integrate with β-receptor adenylate cyclases are activated and make ATP into cAMP.The latter activates ROC and Ca2+ outside cells enter into the cytoplasm. When the amounts of NE reduces and activity of AC declines ROC closes up and stops inward flow of Ca2+.
(2) Na+- Ca2+ exchange
Na+- Ca2+ exchange is also protein on the cellular membrane. Its efficiency of exchange is far higher than Ca2+ pump. When potential within membrane is positive Na+ is outward flow and Ca2+ inward flow.
The role of Ca2+ inward flow is not only enhancing concentration of Ca2+ in cytoplasm but also inducing SR to release Ca2+ .
Myocardial hypertrophy
Acidosis
Decrease of β-receptor and NE
Declined sensitivity of β-receptor to NE
Hyperkalemia K+inhibiting inward flow of Ca2+ competetively
Decrease of Ca2+ inward flow
Dysfunction of excitation-contraction coupling
3) Disorder of combination between Ca2+ and troponin
Acidosis
Ca2+ replaced by H+ to combine with troponin
Decreasing Ca2+ release from SR
Ischemia and hypoxia
Decrease of ATPFall of uptake and release in SR
Decline of Ca2+ concentration in cytoplasm
Dysfunction of excitation-contraction coupling
4, Imbalance growth of myocardial hypertrophy In chronic heart failure excessive hypertrophy of myocardium results in disproportion between increase of myocardial weight and elevation of cardiac function, I.e. Imbalance growth of myocardial hypertrophy and ultimately induces HF.
Mechanism is
1) Increase of myocardial weight exceeding growth of neuraxon in cardiac sympathetic neuron induces fall of distributing density of sympathetic nerve.
3) The amount of capillaries increasing disproportionably with hypertrophy or perfusion disturbance of microcirculation frequently arise ischemia and hypoxia of myocardium
2) The amount of mitochondrion increasing disproportionably with hypertrophy results in insufficiency of energy production of myocardial hypertrophy.
4) Decrease of activity of myosin ATPase in hypertrophy leads to disorder of utilization of energy
5) Disorder of disposal of Ca2+ of SR in hypertrophy conduces dysfunction of excitation-contraction coupling
3.3, Abnormality of ventricular diastole
It is coequal importance for normal cardiac output that both myocardial systole and diastole are all normal. The patients with HF induced by disorder of relaxation may account for 30% of the sum of HF.
1, Delayed restoration of calcium ions
HF
Ischemia of myocardium, severe anemia etc.. Decrease of
ATP
Ca2+ pump not to transport Ca2+ from cytoplasm to the SR and outside the cell adequately
Incomplete relaxation of myocardium
Decrease of affinity between Na+- Ca2+ exchange and Ca2+
Fall of Ca2+
elimination
Disorder of dissociation between Ca2+ and troponin
2, Disorder of disassociation of myosin-actin complex
The myocardial diastole requires not only Ca2+ detaching from troponin but also disassociation of myosin-actin complex. The disassociation of myosin-actin complex is a course of expending energy, I.e.
Myosin-actin complex+ATP
Myosin-ATP + Actin
Decrease of ATP by various factors
Disorder of disassociation of myosin-actin complex
Disturbance of diastole
HF
Thereby;
3, Weakened diastolic potential energy in ventricle of heart
The diastolic potential energy of ventricle is from condition of ventricular systole. The better ventricle contract, the bigger diastolic potential energy of ventricle is. Moreover filling and perfusion of coronary artery in diastole is an concernful factor to promote relaxation of ventricle. Therefore;
Decrease of myocardial contractility by various factors
Stenosis of coronary artery by atherosclerosis or thrombosis
Excessive high pressure within ventricle
Excessive tension in ventricular wall
Reduced perfusion of coronary artery
Disturbance of diastole
Diminished change of geometry structure in heart
4, Declined ventricular compliance
The term of ventricular compliance is defined as the ratio of the change in volume to the change in pressure, “dv/dp”. The ventricular stiffness is the inverse of compliance, I.e., “dp/dv”.
P-V curve can reflect relationship between ventricular compliance and stiffness.
图 心室压力 一 容积( p-V )曲线
N
Causes of decreased compliance have incrassation of ventricular wall by hypertrophy, myocarditis, edema, fibrosis and hyperplasia of stroma, etc..
The clinical significance of decreased compliance is that restricted ventricular relaxation and filling may result in fall of cardiac output and then may induce heart failure.
3.4, Disharmony in contraction and relaxation of heart
Disharmony in contraction and relaxation of heart results in disorder of heart pump and decrease of cardiac output.
The most common cause is arrhythmia.
Section 4
Functional and Metabolic Alteration
in Heart Failure
4.1, Congestion of pulmonary circulationThe congestion of pulmonary circulation is frequently caused by left heart failure. Dyspnea and pulmonary edema are the main representation.
1, Dyspnea1) Exertional dyspneaIt refers to that the patients show dyspnea with increasing movement of physical force and dyspnea can lighten or disappear after a rest.
Causes ;Increased oxygen requirement during movement of physical force
(1) Aggravating hypoxia and CO2 retention
Stimulating respiratory center
(2) Quickened heart rate
Shortened diastole
Fall of perfusion in coronary artery
Hypoxia of cardiac muscle
Decrease of filling in left ventricle
Embittered congestion of lung
(3)Increased blood volume returned to heart
Embittered congestion of lung
Declined compliance of lung
Enhanced resistance of ventilation
Dyspnea
2) Orthopnea
This symptom may be defined as dyspnea that develops in the supine position and is relieved by sitting or recumbent position
Causes of mitigating dyspnea;
(1)
(2)
(3)
Sitting positionA part of blood flow transfering to the lower extremities by gravity
Lightened congestion of lung
Sitting position
Sitting position
Downward movement of diaphragmatic muscle
Increase of vital capacity
Decreased absorption of edematous fluid from the lower extremities
Lightened congestion of lung
3) Paroxysmal nocturnal dyspnea
The patients awakens with a feeling of extreme suffocation during sleep, sits bolt upright, and grasps for breath. When accompanies with wheezing sound it is called “cardiac asthma”. It is a typical manifestation of left heart failure.
Causes ;
(1)
(2)
(3)
The patients by supine position
Dereased volume of thoracic cavity
Fall of ventilation
During sleep Excitation of vagus Contraction of bronchus
Increased resistance of respiratory tract
During sleep Correspondingly depressing of CNS
Dulling of respiratory center
2, Pulmonary edema
It is the most severe manifestation for acute left heart failure.
Mechanism ;1) Rise of capillary pressure----> 30mmHg(4kPa)
2) Increase of permeability in capillaries
Caused by left heart failure or improper fluid transfusion during LHF
Caused by hypoxia
4.2, Congestion of systemic circulation
It is induced by whole or right heart failure.
1, Venous congestion and increase of venous pressure
The main representations are jugular venous engorgement, positive hepatojugular reflux test, etc..
2, Edema
Cardiac edema
3, Hepatomegaly and abnormality of liver function
The patients of hepatomegaly almost account to 95-99% of sum in right heart failure. The chronic right HF may result in cardiogenic hepatocirrhosis.
4.2, Insufficiency of cardiac output
1, Pale of skin or cyanosis
2, Fatigue and adynamia, insomnia, lethargy
3, Decrease of urine volume
4, Cardiogenic shock
Section 5
Treatment Principle of HF
5.1, Preventing and Treating causes, Removing predisposing causes
5.2, Improving function of systole and diastole
1, Elevating function of systole in myocardium
2, Meliorating function of diastole in myocardium
Usage of foxglove, dopamine etc..
Application of calcium antagonism, β-receptor retarder, etc..
5.3, Lightened preload and afterload of heart
1, Reducing afterload of heart
Usage of drug of vasodilatation, e.g., hydralazine, ACEI , calcium antagonism, etc..
2, Modulating preload of heart
Usage of drug of venous vasodilatation, e.g., glonoin, etc..
5.4, Control edema
4, Declined ventricular compliance
The term of ventricular compliance is defined as the ratio of the change in volume to the change in pressure, “dv/dp”. The ventricular stiffness is the inverse of compliance, I.e., “dp/dv”.
P-V curve can reflect relationship between ventricular compliance and stiffness.
Diastolic P
ressure
Diastolic Volume
ab c
A—decline of compliance
B--- normal of compliance
C--- elevation of compliance
Diagrammatic representation of P-V curve in ventricular diastole