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Heart failure
Heart failure is the normal venous return in the case, because the primary cause of heart damage reduction efforts; can not meet the Organization metabolic syndrome in need.
Myocardial contractility decreased cardiac output can not meet the metabolic needs of the body, organs, tissue blood hypoperfusion, pulmonary and systemic congestion as the main performance. Rarely is the diastolic heart failure. So many called congestive heart failure.Frank starling mechanism of left ventricular function curve, the candidates to understand its meaning.
Cardiac hypertrophy, cardiac compensatory remodeling that is, when the hypertrophy sufficient to overcome the wall stress, irreversible left ventricular dysfunction.
Neurohumoral compensatory mechanisms, neuroendocrine activation can enhance myocardial contractility to increase cardiac output, peripheral vasoconstriction, increased Shuinazhuliu heavier burden on the heart.
1) sympathetic nerve activity increased.
2) renin angiotensin system activation.
3) heart failure of various humoral factors change
ANP has a strong diuretic effect.
play vasoconstrictor vasopressin, anti-diuretic, increasing the role of blood volume.Active diastolic dysfunction on left ventricular pressure volume curve shift. Ca2 due to inadequate supply of energy can not be promptly returned and the sarcoplasmic reticulum caused by extracellular pump.
As the compliance decreased and ventricular filling obstacles, it is mainly found in ventricular hypertrophy, such as hypertension and hypertrophic cardiomyopathy time.
Types of heart failure
1. Left heart failure, right heart failure and full of heart failure
2. Acute and chronic heart failure
3. Systolic and diastolic heart failure1) ischemic myocardial injury: segmental myocardial damage in myocardial ischemia in coronary heart disease and myocardial infarction, myocarditis, dilated cardiomyopathy, hypertrophic and restrictive cardiomyopathy.
2) myocardial metabolism disorders: heart disease such as diabetes, heart disease, vitamin B1 deficiency and cardiac amyloidosis.
Cardiac overload
1) before the overload: heart valve regurgitation, blood reflux, such as aortic valve insufficiency, mitral insufficiency, etc.; arteriovenous shunt, heart or cardiovascular diseases such as congenital atrial septal defect or ventricular septal defect, patent ductus arteriosus, etc.; accompanied by an increase in systemic blood volume or circulating blood volume increased arterial diseases such as chronic anemia, arteriovenous fistula, beriberi, etc., thyrotoxicosis, cardiac volume load will inevitably increase. Increase the load capacity of the early compensatory ventricular cavity to expand in order to maintain normal cardiac output, but beyond a certain limit appears decompensation performance.
2) after the overloading: seen in hypertension, aortic stenosis, pulmonary hypertension, pulmonary valve stenosis and left and right ventricular systolic ejection increased resistance to disease. To overcome the increased resistance, compensatory ventricular hypertrophy to ensure the radio output, long-lasting overload, myocardial structure and function of inevitable changes to the final decompensation, cardiac output decreased.
2. Incentives
Infection of respiratory tract infections are the most common and most important incentive; infective endocarditis as a failure of the incentive is not uncommon, often easily understood because of its insidious onset missed. Systemic infection, but one of the incentives.
Arrhythmia, atrial fibrillation and other tachyarrhythmias and severe heart failure can induce arrhythmia.
Water and electrolyte disturbance, such as blood volume increases too much into the sodium, intravenous fluids too much too fast and so on.
Excessive physical exertion or emotional excitement, such as late pregnancy and delivery process, rage and so on. Can increase the heart load.
If not properly treated properly disable the digitalis drugs or antihypertensive drugs, such as excessive diuresis.
Increase the original heart attack or coronary heart disease complicated by other diseases such as myocardial infarction, rheumatic valvular disease appear rheumatic activity, hyperthyroidism or anemia.
Rapidly changing environmental climate.
Classification of heart function.
Mainly based on patient self-conscious activity is divided into four levels:
Class I: People with heart but activity is not restricted, usually does not cause general activity fatigue, palpitations, dyspnea, or angina.
Grade : heart disease was limited physical activity, rest, no symptoms, but usually occurs under general activity fatigue, palpitation, dyspnea or angina.
Grade : heart disease was limited physical activity, usually less than the general activities that have caused the symptoms.
Grade : cardiac patients can not engage in any physical activity. Resting heart failure symptoms also appeared, after the increase of physical activity.
The second is an objective assessment that based on objective examination methods such as ECG, stress test, X ray, echocardiography, and other variables to assess the severity of heart disease, divided into A, B, C, D four levels:
A grade: no objective evidence of cardiovascular disease.
B grade: The objective examination showed mild cardiovascular disease.
C Grade: moderate objective evidence of cardiovascular disease.
D: the performance of serious cardiovascular disease.
Chronic heart failure, in our country, the primary cause of valve disease, hypertension and coronary heart disease second.
1. Clinical manifestations
To left heart failure the most common cardiac output and pulmonary congestion and reduce the performance-based.a. exertional dyspnea: the first is left heart failure symptoms, breathing difficulties caused by the increased level of physical activity reduced heart failure. Higher in patients taking the seat left heart failure, the more serious note.
b. orthopnea.
c. Paroxysmal nocturnal dyspnea: cardiac asthma.
d. of acute pulmonary edema: is left ventricular failure the most serious form of breathing difficulties.
cough, sputum, hemoptysis: cough, sputum and bronchial alveolar congestion is due to start usually occurs at night, when sitting or standing position relieve cough, sputum white foam for serous features. Even visible blood stained sputum. Chronic pulmonary venous congestion pressure increases, plasma can be outside the infiltration of alveolar foam pink sputum. Lead to pulmonary circulation and bronchial collateral circulation formed between the expansion of the bronchial mucosa formed blood vessels, such vessels can cause massive hemoptysis when they burst.
weakness, fatigue, dizziness, palpitation, these are inadequate cardiac output, organ, tissue hypoperfusion, and compensatory and accelerated heart rate, the main symptoms.
oliguria and renal dysfunction symptoms signs of chronic heart failure patients with left-general had enlarged heart, pulmonary valve area of the second heart sound diastolic apex hyperthyroidism and gallop.
Right heart failure in the performance of the main body of venous congestion.
1) Symptoms
gastrointestinal symptoms of abdominal gastrointestinal tract, liver congestion Zhang, loss of appetite, nausea, vomiting, weight gain is the most common symptoms of right heart failure, nocturia, oliguria often appear.
exertional dyspnea secondary to left heart failure in the existing right heart failure dyspnea, right heart failure as a simple shunt due to congenital heart disease or lung disease, also had significant difficulty in breathing.
2) signs
Parts of the body falls edema, gravitational edema, renal edema can be distinguished from the indentation edema, pleural effusion, more common in the whole heart failure, with bilateral common, as more and more to the right of unilateral Zeyi See. More than the sodium and water retention and venous hypertension caused by capillary congestion.
levy JVP jugular vein enhancement, filling, engorgement, hepatic jugular vein reflux and positive signs. Help identify other causes of heart failure and hepatomegaly.
hepatomegaly tenderness: tenderness often accompanied by swelling of the liver due to congestion, persistent chronic right heart failure can cause cardiac cirrhosis, jaundice and a lot of late, there may be ascites.
cardiac signs left sternal border between 3 to 4 to help right heart failure and diastolic gallop right ventricle can be significantly increased due to the emergence of tricuspid regurgitation regurgitation murmur.
pleural effusion and ascites, cardiac ascites and liver cirrhosis, pleural effusion, mostly bilateral, unilateral and more time on the right and left pleural effusion may have pulmonary embolism.
Heart failure
Right heart failure secondary to left heart failure and the formation of the whole heart failure, when the advent of right heart failure and right cardiac output and reduction of the paroxysmal symptoms of breathing difficulties but slightly reduced pulmonary congestion. Dilated cardiomyopathy, such as performance for the left and right ventricular failure and who also, pulmonary congestion symptoms are often not very serious, the performance of left heart failure is mainly related to reduced cardiac output symptoms and signs of apical gallop, pulse pressure reduction .
2. Should have a clear diagnosis of the first diagnosis of structural heart disease. The symptoms of heart failure is an important basis for diagnosis of heart failure. Fatigue, weakness and other cardiac output decreased because the symptoms are nonspecific, diagnosis of little value. The left lung congestion caused by heart failure of different degrees of difficulty breathing, circulation of right heart failure caused by congestion jugular vein distention, hepatomegaly, and edema, an important basis for the diagnosis of heart failure.
3. Differential diagnosis
Bronchial asthma: more common in the elderly cardiac asthma had a history of hypertension or chronic heart valves, bronchial asthma, allergies more common in young people; the former attack must sit up, severe pulmonary rales dry of mouth, or even pink sputum color foam, which is not necessarily forced to sit up white phlegm cough can often relieve dyspnea, pulmonary auscultation to wheeze based.
Pericardial effusion, constrictive pericarditis, due to the superior vena cava obstruction can also cause liver return to a large, lower extremity edema, such as performance, should be based on medical history, heart and peripheral vascular signs were identified, echocardiography can be confirmed.
Lower extremity edema associated with liver cirrhosis and chronic right heart failure should be identified, in addition signs will help identify the basis of heart disease, the non-cardiac cirrhosis of the liver will not appear on the vena jugular vein distention and other signs of venous obstruction. This is a very important differential points.1) increase exercise tolerance, improve quality of life rest, restricted physical activity, do not advocate complete bed rest to prevent pulmonary embolism in venous thrombosis.
control of sodium into the
Application of diuretics, including diuretics and potassium-sparing diuretics row role in distal convoluted tubule proximal preparations. Potassium-sparing diuretics, including the role of the distal convoluted tubule and distal collecting duct preparations.
a. thiazide diuretics: to hydrochlorothiazide as the representative, acting on the renal distal tubule, inhibiting sodium reabsorption. As a sodium potassium exchange also reduces the absorption of potassium. To the effect of diuretics, mild heart failure may be the preferred drug, thiazide diuretics can inhibit the excretion of uric acid, causing hyperuricemia, may also interfere with metabolism of glucose and cholesterol, long-term application of attention to monitoring.
b. loop diuretics: furosemide, represented by acting on the medullary ramus half Woo, also in the row row sodium potassium, as potent diuretic. Hypokalemia is the main side effects of these diuretics, potassium must be noted.
c. potassium-sparing diuretics: commonly used are:
Spironolactone: role of the renal distal tubule, interfering role of aldosterone, the increased absorption of potassium ions, while the natriuretic, diuretic effect, but not strong. With thiazide or loop diuretics in combination can enhance and reduce the potassium loss diuretic.
Triamterene: direct role in the renal distal tubule, sodium potassium row, diuretic effect is not strong. Common row of potassium diuretics, potassium play a role.
Ami Norian: mechanism of action similar with triamterene, a diuretic effect can produce a strong hyperkalemia. General and Pai potassium-sparing diuretics are combined, the occurrence of hyperkalemia is unlikely, but not while taking potassium.
Electrolyte imbalance is most prone to long-term use of diuretics side effects, especially hyperkalemia or hypokalemia can lead to serious consequences, should be closely monitored. Angiotensin-converting enzyme inhibitors have a stronger role in potassium, with different types of diuretics with caution.
Note: a. row of potassium-sparing diuretics should be used intermittently, application of potassium-sparing diuretics should be continued
b. exclusive combination of potassium and potassium-sparing diuretics do not generally separable potassium supplement.
c. renal failure, disable the potassium-sparing diuretics, loop diuretics should be selected
d. Note that low potassium, low magnesium, hyponatremia, water disorder.
e. Note the interaction between drugs: such as indomethacin may be against the furosemide effect.
Application vasodilator
a. venular dilator: a small volume of blood veins is even a slight expansion can also reduce the effective circulating blood volume and lower change thy blood. With the reduction of blood volume change thy, left ventricular end diastolic pressure and pulmonary circulation pressure decreased, pulmonary congestion relief. But can not increase cardiac output in clinical practice with nitrate-based formulations. Such as nitroglycerin.
b. Small artery vasodilator: the peripheral vascular resistance decreased, left ventricular ejection function improved cardiac output increase will help reduce the ventricular load, left ventricular end diastolic pressure and the corresponding decline in pulmonary vascular pressure, lung congestion and improve , the proper treatment of the surrounding vascular resistance decreased, while cardiac output increased, while blood pressure did not change significantly.
Expansion of the drug a lot of small arteries. Receptor antagonist [prazosin, Siniora to Haier], direct relaxation of vascular smooth muscle preparations (two-hydralazine), nitrate preparations, calcium channel blockers and angiotensin converting enzyme inhibitors. For those who rely on elevated left ventricular filling pressure to maintain cardiac output obstructive valvular heart disease, such as mitral stenosis, aortic stenosis and left ventricular outflow tract obstruction should not be applied in patients with potent vasodilators, and For valvular reflux disease can be applied.
3) increased cardiac output:
Digoxin digitalis drugs can significantly improve symptoms, improve exercise tolerance, reduced hospitalizations, increased cardiac output, but the final survival rate observed digoxin group and no difference between the control group.
Positive inotropic effect mainly through inhibition of Na + on the myocardial cell membrane refractory heart failure and irreversible heart failure treatment: refractory heart failure should strive to identify potential causes, and try to correct, such as rheumatoid activity, anemia, heart infection meningitis, electrolyte disturbance, hyperthyroidism, digitalis overdose, recurrent pulmonary embolism and other small areas. Independent of whether patients suffering with heart and other diseases such as tumors. Simultaneous adjustment of heart failure medication, diuretics and vasodilators potent inotropic agents and joint applications. Edema of highly refractory to try the blood ultrafiltration.
Most of the patients with heart failure is not reversible cause can not be corrected, and its the only way out is heart transplantation.


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