What is Cardiac Failure or Heart Failure? (Section 2)

Heart Failure Definition and Meaning: Heart failure refers to the development of cardiovascular disease to a certain degree, weakened myocardial contractility or diastolic dysfunction, reduced cardiac output, which can not meet the body’s tissue and cell metabolism needs. At the same time venous blood flow is blocked, venous system stasis and blood Dynamics changes in neurohumoral fluids resulting in a series of symptoms and signs. It is similar as cardiac arrest or cardiac failure, though not the same. According to the development process of heart failure, it is divisible into acute and chronic heart failure, and according to cardiac systolic and diastolic dysfunction. It is divisible into systolic heart failure and diastolic heart failure. 

 

 Chronic Heart Failure

Cause: The 5 determinants affecting cardiac output are:

i.                  The preload of the heart

ii.               The postload

iii.            Myocardial contractility

iv.             Heart rate

v.                Coordination of myocardial contraction.

Changes in one or more of the above factors can affect heart function and even heart failure.

 

I. The basic cause of Cardiac Output

 (1) Excessive pre-load ventricular diastolic return blood volume such as aortic or mitral regurgitation, ventricular septal defect and arterial duct occlusion can all overload the left ventricle during diastole, leading to the left heart Failure. Congenital atrial septal defect can overload the right ventricle during diastole, leading to right heart failure. Diseases of high cardiac output such as anemia and hyperthyroidism, due to the increase in return blood volume, increases the diastolic load of the left and right ventricles, leading to total heart failure.

 

(2) Post-load overload such as hypertension, aortic valve stenosis or obstruction of the left ventricular outflow tract, exacerbates the left ventricular systolic load which can lead to left heart failure. Pulmonary hypertension and obstruction of the right ventricular outflow tract obstruct the right ventricular systolic load which can lead to right heart failure.

 

(3) The weakening of myocardial contractility is common such as myocardial ischemia or necrosis caused by coronary atherosclerosis, myocarditis (viral, immune, toxic, bacterial) of various causes and myocardial diseases of unknown cause. Severe anemia heart disease and hyperthyroid heart disease, etc. myocardial contractility can become significantly weak, leading to heart failure.

 

(D) Uncoordinated ventricular contraction: Coronary heart disease Severe myocardial ischemia leads to weak or contracted myocardial contraction, such as ventricular aneurysm.

 

(5) Reduced ventricular compliance: For example, ventricular hypertrophy and hypertrophic cardiomyopathy. When ventricular compliance is significantly reduced, it can affect ventricular relaxation and affect cardiac function.

 

Inducing factors of Cardiac Output

 (1) Infections Prions and lung infections are common causes of heart failure. In addition to infections that can directly damage the heart muscle, fever can increase heart rate and increase heart load.

 

(2) Excessive physical labor or emotional excitement.

 

(3) Arrhythmia: Especially tachyarrhythmia such as paroxysmal tachycardia, atrial fibrillation, etc. can increase the heart load, reduce the amount of cardiac output and cause heart failure.

 

(4) Pregnancy and childbirth: The blood volume of pregnant women increases during pregnancy. Due to the contraction of the uterus during delivery, the volume of returning blood is significantly increased, and the force during delivery increases the heart load.

 

(5) Infusion (or rapid or excessive blood transfusion): excessive input of fluid or sodium, sudden increase in blood volume, overload of the heart and induction of heart failure.

 

(6) Severe anemia or hemorrhage can cause myocardial ischemia and hypoxia, increase heart rate and increase heart load.

 

Pathogenesis and Pathophysiology of Heart Failure

The development process of heart failure is divisible into cardiac function compensation period and decompensation period.

 

A. Cardiac function compensation period

The heart has a large reserve power. When the diseased heart load increases and the cardiac output decreases, the heart can compensate by the following ways to increase the cardiac output even closer to normal. This is the compensatory period of cardiac function.  The ways to play a compensatory role are:

 

(1) Sympathetic nerve excitement and cardiac insufficiency at the beginning, decreased cardiac output, lower blood pressure stimulates the aorta body and carotid sinus baroreceptors. At the same time increased ventricular end-diastolic pressure and blood volume stimulated atrial and large vein pressure sensors, both of which can cause sympathetic nerves to reflexively, strengthen myocardial contractility, increase heart rate and increase cardiac output.

 

(2) Increased ventricular end-diastolic volume: Due to sympathetic nerve excitement, the release of catecholamines increases the contraction of blood vessels in various tissues and organs of the body, including resistance vessels and volume vessels, to redistribute blood volume to ensure heart, brain, etc. Volume vasoconstriction reduces blood volume and increases venous pressure, so the amount of blood returned to the heart increases. In addition, the activity of the renin-angiotensity-aldosterone system increases, which enhances the reabsorption of sodium and water by the kidneys. This increases the extracellular fluid and blood volume and increases the amount of blood returned to the heart. Frank-Starling’s law, that is, an increase in ventricular diastolic volume in a certain range can strengthen the contractile force of the heart muscle and thus increase the stroke volume.

 

(3) Myocardial hypertrophy: When the persistent capacity load or pressure load increases, the myocardial hypertrophy and the number of sarcomerees in the functional unit of myocardial contraction increase, so the myocardial contractility strengthens.

 

Through the above compensation function, the cardiac output increases, which can still meet the tissue metabolism needs of the human body during moderate physical work without the symptoms of blood stasis. This is referable as the cardiac function compensation period.

 

B. Heart decompensation period

When the heart disease continues to worsen, and cardiac function declines beyond its compensatory function, cardiac decompensation occurs. The main pathophysiological changes are:

 

(1) Increased heart rate, decrease in cardiac output, early heart failure, compensatory heart rate, although it helps to increase cardiac output to or near normal levels. However, accelerated heart rate also increases myocardial oxygen consumption. Moreover, the coronary blood supply and ventricular filling time shorten, the stroke volume is decreases and the cardiac output is reduces.

 

(2) The reduction of heart and blood flow that water and sodium causes, leads to redistribution of blood and decrease of renal blood flow. Decrease in renal blood flow can reduce glomerular filtration rate or increase renin secretion, which in turn acts on angiotensinogen that the liver produces and forms angiotensin I. Angiotensin passes through the lung and kidney circulation, and forms angiotensin under the action of invertase. The latter not only causes systemic and renal arteriolar spasm to aggravate renal ischemia, but also promotes the adrenal cortex to secrete more aldosterone. The result is Increase in sodium retention, increase in plasma osmotic pressure, osmotic pressure sensors stimulation near the supraoptic nucleus of the hypothalamus, and reflectively increased the secretion of antidiuretic hormones in the posterior pituitary gland. This causes sodium and water retention, increase in blood volume, veins and capillaries Hyperemia, and increased stress.

 

(3) Increased end-ventricular pressure: In heart failure, myocardial contractility decreases, stroke volume decreases, residual blood volume in the ventricular cavity increases, end-ventricular pressure increases, venous return is blocked, causing venous stasis and venous pressure. When the hydrostatic pressure in the capillaries increases beyond the osmotic pressure of the plasma and the tissue pressure, the extravasation of the fluid inside the capillaries and the tissue edema.

 

Clinical Manifestation of Cardiac Arrest

The clinical manifestations of heart failure are closely related to which ventricle or atrial involvement. The clinical features of left heart failure are mainly due to pulmonary stasis and pulmonary edema that left atrium and / or right ventricular failure causes. The clinical features of right heart failure are due to systemic venous blood stasis due to right atrium and / or right ventricular failure and Water and sodium retention. After the occurrence of left heart failure, the right heart also often suffers functional damage in succession, eventually leading to total heart failure. In the presence of right heart failure, we may see reduction in symptoms of left heart failure.

 

I. Left heart failure

(A) Dyspnea is the earliest and most common symptom of left heart failure. Mainly due to acute or chronic pulmonary stasis and reduced vital capacity. The lighter has dyspnea only during heavy physical work and disappears quickly after rest, so it is called manual dyspnea. This is due to the increase in the amount of blood returned to the heart due to labor. When the right heart function is normal, the blood stasis in the lungs is aggravated. With the progress of the disease, mild physical activity will cause dyspnea and severe patients will also feel dyspnea at rest. Thus, they are forced to take a semi-recumbent or sitting position, referable as sit-side breathing (forced breathing). Because the seat can make the blood affected by gravity, it accumulates in lower sagging parts such as the lower limbs and abdomen. There is reduction in back blood volume in comparision to when lying down, and the pulmonary congestion is reduced. At the same time, the diaphragm is reduced when sitting and the lung capacity is increased, which makes breathing difficult.

 

Paroxysmal nocturnal dyspnea is a manifestation of left heart failure. Patients often wake up in deep sleep, have a sense of suffocation, are forced to sit up, cough frequently and experience severe breathing difficulties. A few minutes after sitting up the symptoms disappear. In severe cases, cyanosis, cold sweat and wheezing can be heard in the lungs, which is called heart asthma. In severe cases, it can develop into pulmonary edema, a large amount of foamy bloody sputum, wet lungs in both lungs, blood pressure can drop and even shock.

 

(B) Cough and hemoptysis are common symptoms of left heart failure. The cause is congestion of the alveolar and bronchial mucosa, which often coexist with dyspnea, hemoptysis foamy or bloody sputum.

 

(C) Other ailments may include fatigue, insomnia, and palpitations. Heavy breathing, lethargy, dizziness, loss of consciousness and convulsions can occur during severe cerebral hypoxia.

 

(D) Signs In addition to the original signs of heart disease, there may be diastolic galloping rhythms in the apical area, second heart sounds in the auscultation area of ​​the pulmonary valve, and moist rales can be heard at the bottom of the two lungs. The sounds accompany wheezing sounds, often with alternating pulses.

 

II. Right heart failure

(A) Stomach fullness is an early symptom of right heart failure. Often accompany loss of appetite, nausea, vomiting and upper abdominal pain, which are mostly caused by congestion of the liver, spleen and gastrointestinal tract. The liver has congestion, is swollen and tender, and those with acute congestive liver in acute right heart failure have sharp upper abdominal pain and can be misdiagnosed as acute abdomen. Chronic hepatic congestion and hypoxia can cause degeneration and necrosis of liver cells, and eventually develop into cardiogenic cirrhosis, abnormal liver function or jaundice. If tricuspid insufficiency coexists, dilated pulses may be felt upon palpation of the liver.

 

(2) The jugular vein irritation is a more obvious sign of right heart failure. Its appearance is often earlier than subcutaneous edema or hepatomegaly. At the same time, superficial veins such as the sublingual and arm are abnormally filled. When the liver with congestion and enlargement is compressed, the jugular veins are more swollen.

 

(3) Edema: Early in right heart failure, due to the retention of sodium and water in the body, there is an increase in body weight before the emergence of edema. Edema occurrs when fluid retention reaches more than five kilograms. Heart failure edema mostly appears in the lower extremities. Bedridden patients often have low-hanging parts such as waist, back and crotch. They are depressed edema which can affect the whole body in severe cases. Lower limb edema appears or worsens in the evening, which reduces after a rest or disappear, often accompanied by an increase in the amount of urine at night. This is because the amount of returning blood at night is less than that during daytime activities. The heart can still pump blood from the venous return. The residual blood volume at the end of ventricular contraction significantly reduces. Increased capillary pressure alleviates, so edema is reduces or subsides.

 

A few patients may have pleural fluid and ascites. Pleural effusion can be seen in the left and right thoracic cavity at the same time, but the right side is more. The reason is not clear. Because the parietal pleural veins return to the vena cava, the visceral pleural veins return to the pulmonary veins. Most of the ascites occurs in the late stages, mostly due to cardiogenic cirrhosis.

 

(4) Asters with cyanotic right heart failure mostly have cyanosis in different degrees. They are first seen on the fingertips, lips and auricles and are more obvious than those with left heart failure. The reason is that in addition to the lack of oxygenation of hemoglobin in the lungs, the blood flow is often slow and tissues take more oxygen from capillaries to increase the reduction of hemoglobin in the blood (peripheral cyanosis). Severe anemia is not obvious.

 

(5) Symptoms of the nervous system: There may be symptoms such as nervousness, insomnia and lethargy. In severe cases, mental disorders may occur, which may be caused by cerebral congestion, hypoxia or electrolyte disorders.

 

(6) Heart signs are mainly the original heart disease manifestations. Because right heart failure is often secondary to left heart failure, both the left and right hearts can have enlargement. When the right ventricle enlarges and causes tricuspid regurgitation, a tricuspid auscultation can be heard at the tricuspid auscultation. Symptoms of pulmonary congestion caused by left heart failure and secondary heart sounds in the pulmonary valve area can be alleviated by the presence of right heart failure.

 

III. Total heart failure

There may be clinical manifestations of left and right heart failure at the same time, and the clinical manifestations of left or right heart failure may be the main.

 

Laboratory and other inspections for Left Heart Failure

1. X-ray left heart failure can show enlarged heart shadows, thickening of blood vessels in the upper lung field, fine veins in the lower lung field, red blood distribution in the pulmonary veins, increase in hilar shadows and pulmonary interstitial edema. The lung lobules became thicker, and a horizontal Kerley’s B line is visiuble in the lower field of both lungs. Acute pulmonary edema, significant hilar congestion and a butterfly cloud shadow. The right vena cava dilatation can be visible in right heart failure.

 

2. The electrocardiogram can appear left ventricle, right ventricle or left and right ventricular hypertrophy ECG graphics.

 

3. Hemodynamic monitoring: Except for mitral stenosis, the measurement of pulmonary capillary wedge pressure can indirectly reflect the left atrial pressure or left ventricular filling pressure, and the average pressure of pulmonary capillary wedge pressure. The normal value is 0.8-1.6. kpa (6-12mmHg), higher than 2kpa (15mmHg) often suggest left heart failure, higher than 4.8kpa (36mmHg), suggesting that acute pulmonary edema may be imminent. The normal value of central venous pressure is 0.588-1.176 (6-12cmH2o). In right heart failure, the central venous pressure can increase.

 

Diagnosis of Congestive Heart Failure

First, the diagnosis of congestive heart failure: There is a previous history of heart disease, and left heart or right heart failure symptoms and signs are not difficult to diagnose. X-ray examination of the heart and lungs is also helpful for diagnosis. If necessary, expert can perform hemodynamic monitoring to confirm the diagnosis.

4 Stages of congestive Heart Failure Chart

 

Second, the determination of the degree of heart failure clinically divisible into four levels according to the patient’s heart function status. If divided by heart failure, it is divisible into three degrees, the second level of heart function is equivalent to one degree of heart failure, and so on.

 

Cardiovascular disease occurs at the level of cardiac function, but all work has no restriction (asymptomatic).

 

Heart function level two (Heart failure I degree) is capable of general daily labor, but heavier physical activity can cause heart palpitations, shortness of breath and other symptoms of heart dysfunction.

 

Heart function III (heart failure degree) without any discomfort at rest, but the heart dysfunction manifested during ordinary daily activities.

 

Any activity of the fourth grade of heart function (III degree of heart failure) is symptomatic, even when bed rest, there are symptoms of heart insufficiency.

 

Differential diagnosis

I. Differentiation between cardiac asthma and bronchial asthma. The former is more common in middle-aged people. It has a history of heart disease and signs of heart enlargement. It often occurs at night. The lungs can smell dry and wet rales, which is effective for heart-tightening agents. There is no history of heart disease and heart signs, happens often in spring and autumn. A history of allergies, lungs filled with wheezing, effective on ephedrine, adrenal corticosteroids and aminophylline is possible.

 

Second, the identification of right heart failure and pericardial effusion, constrictive pericarditis, etc. All three can appear liver enlargement, ascites, but right heart failure is often accompanied by heart murmur or emphysema, enlarged heart when pericardial effusion. The voiced sound world can vary with body position, the heart sounds are distant, there are no murmurs and strange pulses. The constrictive pericarditis is not large or slightly larger, no noise and has strange pulses.

 

Heart Failure Treatment

I. Treatment of heart failure

(A) reduce the load on the heart

1. Rest: Arrange the patient’s life, activities and rest appropriately according to the condition. Patients with mild heart failure can only limit their physical activity to ensure adequate sleep and rest. People with more severe heart failure should stay in bed, including proper mental rest. Beware of improved function, encourage the patients to gradually resume physical activity as soon as possible according to individual circumstances. For patients with excitement and irritability, give sedatives such as diazepam and rimienin as appropriate. Use it with caution in elderly or severe patients, especially those with emphysema.

 

2. Controlling sodium salt intake and reducing sodium salt intake can reduce water retention in the body and reduce the heart’s preload, which is an important measure for the treatment of heart failure. In patients with moderate and severe heart failure, there should be limit on the sodium salt to 0.5-1.0g and equivalent to 1-2.5g of salt. After heart failure control, give a low-salt diet. Limit the sodium salt intake to 2-3g (equivalent to 5-7g). In a large number of diuretic patients, there is no need to strictly limit salt.

 

3. The application of diuretics can make the body retain too much fluid to discharge, reduce edema of tissues and organs throughout the body, reduce excessive blood volume and reduce the preload of the heart.

 

Commonly used diuretics

(1) At present, thiazines are commonly usable as diuretic urine plugs, chlorthalidone, etc., which are oral diuretics. After one hour of treatment, a curative effect occurs, which mainly acts on the proximal tubules of the kidney and inhibits sodium and chlorine reabsorption. The excretion of sodium, potassium and chlorine increases, and prolonged use is prone to produce hypokalemia. Therefore, add or use potassium chloride or potassium diuretics intermittently.

The dosage is: 25-50 mg of dihydrodiuretic urine 3 times a day.

100-200 mg of chlorthalidone once every other day.

 

(2) Diuretics: The effect of diuretics is fast and strong. Intravenous injection can produce a diuretic effect within 5-10 minutes, reaching a peak in 1 hour. It is suitable for acute left heart failure or refractory heart failure. Because it acts on the ascending branch of Henri’s ridge, preventing sodium and chlorine from absorption, a large amount of diuresis can cause hyponatremia, hypokalemia, hypochlorinated limulus poisoning, or circulatory failure due to excessive reduction in circulating blood volume.

The dosage is: 20-40 mg of furosemide orally, 2-3 times a day, intramuscularly or intravenously, 1 or 2 times a day.

25-50 mg of sodium urate, intravenously, once a day. The side effects are the same as those of fast urine and those who are resistant to fast urine can be used at a dose of 1 mg twice daily, orally.

 

(3) Potassium-preserving diuretics act on the tubules of the far bend, excrete sodium and retain potassium. The diuretic effect alone is poor. It is often use is in combination with other potassium-releasing diuretics to improve the diuretic effect and reduce the side effects of electrolyte disturbances. Those with renal insufficiency should use with caution. 4 times, ampicillin 50mg 3 times a day, orally.

 

(4) Carbonic anhydrase inhibitors: Commonly used acetazolamide, which has a less diuretic effect, mainly inhibits carbonic anhydrase in renal tubular cells, hinders sodium-hydrogen exchange, and excretes sodium, potassium, and bicarbonate to diuretic.

General dose: 0.25-0.5g, once a day orally.

 

Attention should be paid when using diuretics

(1) The choice of diuretics should be determined according to the condition. Mild heart failure can use thiazide diuretics and potassium supplementation. Moderate heart failure can choose thiazines and potassium diuretics. If it is ineffective, use diuretics Agent. In severe heart failure diuretics and potassium diuretics should be preferable. Those who have no satisfaction with the effect can add adrenal corticosteroids.

 

(2) Combined use and intermittent use: Use in combination can maximize the diuretic effect and reduce side effects. Intermittent medication allows antibodies to have time to restore electrolyte balance, which can improve efficacy.

 

(3) Handle electrolyte disorders such as hyponatremia and hypokalemia in a timely manner.

 

(4) Pay attention to the interaction of other drugs, such as the application of indomethacin, which may antagonize the action of furosemide by inhibiting the synthesis of prostaglandins.

 

4. The application of vasodilators: The basic principle of vasodilators in the treatment of heart failure is to improve heart function by reducing pre- or (and) post-load. In heart failure, due to decrease in cardiac output and reflex sympathetic-adrenal system excitement, peripheral blood vessels constrict, left ventricular ejection impedance increases, and postload increases. Application of small arterial dilators such as hydrazine and pyridazine can reduce arterial pressure and reduce left ventricular ejection impedance, thus increasing cardiac output and cardiac output. The use of volume vasodilators such as nitroglycerin and isosorbide dinitrate can directly expand the volume of blood vessels, increase the volume of the venous system, reduce venous tension and reduce return to right heart blood. This thereby reducing ventricular end-diastolic pressure and reducing Load, ventricular wall tension decreases during ventricular contraction, and myocardial oxygen consumption decreases, which is conducive to improving cardiac function.

 

There are many types of vasodilators in common use, which can be divisible according to their main mechanism of action:

 

i. Venous dilators, such as nitroglycerin and nitrates

Small arterial dilators, such as hydrazine benzimidazine, minolopidine, etc. Arterial and venous dilators, such as sodium nitroprusside, phentolamine, prazosin, and meproproline. Intravenous dilatation can reduce afterload.

 

Phentolamine is an alpha adrenergic inhibitor, which can relax vascular smooth muscle directly. It has dilatation effect on arterioles and veins, but it has stronger expansion of arterioles, so it can reduce peripheral vascular resistance and increase venous blood volume. Reduce left ventricular filling pressure, thereby increasing stroke volume and cardiac output and improving left ventricular function. The dosage varies from person to person. Generally, 10-20mg of phentolamine is added to 250ml of 10% glucose solution, which slowly drips into the vein, starting at 0.1mg / min, and 0.1mg / min is added every 10-15 minutes. Urgent patients can also use 3mg to add 20-40ml glucose solution, slow intravenous injection at the rate of 0.1-0.2mg per minute. The medication process should be closely observed to prevent hypotension.

 

Sodium nitroprusside has the effects of dilating arterioles and veins, thus effectively reducing ventricular anterior and posterior loads. Strong effect, short maintenance time, suitable for hypertension crisis and acute left heart failure caused by various reasons.

Dosage: Add 25-50mg of sodium nitroprusside to 500ml of glucose solution in the dark. Start the dose from 8-16ug per minute and then increased by 5-10ug every 5-10 minutes. The dose should be different from person to person. Pay attention to low blood pressure during application, and measure the blood thiocyanate level for a long time or when a large dose is input. If cyanide poisoning occurs, neurotoxicity symptoms may occur.

 

Nitrate nitroglycerin and isosorbide dinitrate mainly act on the venous system and have a weak effect on resistance arteries. After taking nitrate, it significantly reduces the wedge pressure of pulmonary capillaries and the left ventricular filling pressure, but the cardiac output. There is no significant change in stroke volume. Take Nitroglycerin 0.6mg for only 20-30 minutes, and take 5mg of isosorbide dinitrate for 60-90 minutes.

Captopril is an angiotensin-converting enzyme inhibitor, which reduces angiotensin to angiotensin , reduces aldosterone concentration, reduces vasoconstriction and water and sodium retention and reduces the load on the heart. At the same time, it reduces bradykinin breakdown increases prostaglandin activity, causes blood vessels to dilate and reduces cardiac afterload. The starting dose of commercially available Kaibotong is 6.25mg 3 times a day, without side effects. Increase the dose as appropriate. The main side effect is hypotension.

 

When applying vasodilators, you should closely observe changes in blood pressure and pulse. Hemodynamic monitoring is of great value in guiding the treatment of heart failure and the selection of vasodilators. Floating catheters can be placed as appropriate for hemodynamic monitoring and the treatment plan is determinable according to the patient’s pre- and post-load conditions. Should also pay attention to side effects of the drug.

 

(B) Strengthen myocardial contractility 

1. Application of digitalis drugs: Digitalis cardiac glycosides can directly strengthen myocardial contractility and increase cardiac stroke volume, thereby reducing the residual blood volume at the end of systole and reducing the end-diastolic pressure. This is conducive to the relief of congestion in various organs, urine increase in volume and slow heart rate. The mechanism by which digitalis can increase myocardial contractility is that digitalis inhibits the cell membrane Na + -K + -ATPase and increases intracellular sodium. Na + -Ca ++ exchange tends to be active, Ca ++ influx increases, and myocardial contractility increases.

Although increase in myocardial contractility can increase myocardial oxygen consumption, contraction of the ventricular cavity and decrease in wall tension reduce myocardial oxygen consumption. Therefore, digitalis preparations can improve myocardial working capacity without increasing myocardial oxygen consumption. Secondly, digitalis can slow the atrioventricular conduction directly or indirectly through exciting the vagus nerve. It is usable to treat atrial fibrillation or atrial flutter with rapid ventricular rate. Excessive digitalis on the contrary will reduce myocardial contractility, increase atrioventricular junction area and Purdue fiber autonomy. So it can cause ectopic rhythms and reentry and cause arrhythmia.

 

(1) Indications and contraindications – The indications include:

i. Except for heart failure that digitalis poisoning causes, heart failure due to other reasons can be used.

ii. Rapid supraventricular arrhythmia, such as atrial fibrillation and flutter of rapid heart rate, paroxysmal supraventricular tachycardia and so on.

 

Contraindications are:

i. Heart failure with digitalis poisoning

ii. Preexcitation syndrome with atrial fibrillation or flutter

iii. Obstructive cardiomyopathy, digitalis can aggravate left ventricular outflow tract obstruction, so should not use it. One can still apply it when heart fails.

iv. Atrioventricular block is usable with caution only when accompanied with heart failure. When complete atrioventricular block with heart failure, place a ventricular pacemaker and then use digitalis.

v. Sinus bradycardia with ventricular rate below 50 times per minute, atrial fibrillation or atrial flutter with complete atrioventricular block or ventricular rate below 60 times per minute.

 

(2) Commonly used preparations and their usage Commonly used preparations.

Digitalis preparations commonly used in clinical practice can be divisible into:

i. Fast-acting preparations, such as poisonous trichoside K, G, cedilan, digoxin, etc.

ii. Slow-acting preparations are digitalis leaves, digitalis toxins and so on. There is need to keep in mind the administration route, drug action, half-life, effective therapeutic amount and maintenance amount of these preparations.

 

Preparations selection

Choose the preparation according to the onset of acuteness and severity, such as acute left heart failure. Use fast-acting drugs such as cedilan and poisonous trichoside K. For chronic heart failure, oral digoxin is appropriate. Heart failure with fast heart rate, such as atrial fibrillation with rapid ventricular rate can be treated with cedilan.

Digitalis dose: The positive muscle strength of digitalis has a linear relationship with the dose, that is, as the drug dose in the body increases, the myocardial contractility increases accordingly.

When the patient takes a certain amount of medicine daily, the medicine discharges in a certain proportion. It accumulates in the body in a certain proportion outside the body. When the accumulated drug in the body reaches a certain concentration to obtain the best effect, it is referable as the effective treatment amount. Then a certain amount of drug is given daily to supplement the amount of the drug lost by daily metabolism. This is referable as the maintenance volume. The dosage of digitalis preparations varies widely, so record daily doses detail.

i. Age: Different ages have significant differences in tolerance to digitalis. Elderly people may reduce the ATPase activity of myocardium, increase sensitivity to digitalis, reduce renal function, and reduce renal excretion of glycosides. So the dosage should be small.

 

ii. The state of liver and kidney function: digoxin is excreted through the kidney, so the dosage of digoxin should be reduced in patients with renal insufficiency. Reduce or discontinue it when oliguria or anuria is not present. Digitalis metabolizes in the liver, so the dose in patients with liver dysfunction should also be smaller than constant.

 

iii. Thyroid function: Hypothyroidism, digoxin clearance is reduces, digitalis requirement is reduces. Hyperthyroidism, digoxin clearance increases. Digitalis requirement also increases.

 

iv. Nature and extent of heart disease: Patients with heart failure, such as ischemic heart disease, hypoxic pulmonary heart disease and cardiomyopathy have reduced tolerance to digitalis, especially patients with severe heart failure. Sex is worse.

 

v. Electrolyte disorders: Hypokalemia, hypomagnesemia and hypercalcemia can make the body less tolerant to digitalis.

 

vi. The effects of other drugs: When applying reserpine, guanethidine, amiodarone, quinidine and other drugs together with digitalis, it can increase the sensitivity to digitalis and easily cause poisoning.

 

Administration method: First of all, ask if you have taken digitalis drugs within two weeks and then choose the method of emergency administration according to the severity of the disease.

 

a. Fast-feed: Patient is in critical condition and not used digitalis in the last two weeks. Use 0.4g of cedilan diluted with 20ml of glucose solution and then slowly inject intravenously. After 2 to 4 hours, if necessary, re-intravenous Inject 0.2-0.4mg and then change to oral digitalis to maintain. Or use poisonous trichoside K0.25mg, dilute with glucose solution slowly intravenously, if necessary, then intravenously inject 0.125mg after 2-4 hours. Digoxin oral administration can be given 0.25mg 2-3 times a day according to the situation for the first one or two days. Then maintain the amount after getting good effect.

 

b. The slow-dose method can give a small dose of digoxin to patients with less severe heart failure, which is equivalent to a daily maintenance amount (0.25-0.5mg) after 5 half-lives (one half-life is 1.5 days, that is 1.5 × 5 = 7.5 days), the blood concentration can reach the therapeutic level. This method is relatively safe and effective and the incidence of poisoning is low.

 

The clinical indicators to determine the efficacy of digitalis are those with sinus rhythm:

i. The subjective symptoms improve, the diuretic effect is good and the edema subsides.

ii. The heart rate slows and the heart shadow shrinks

iii. The venous pressure and circulation time return to normal.

iv. The liver shrinks and the tenderness disappears. For those with atrial fibrillation or atrial flutter, the ventricular rate can be reduced to 80 times per minute as an effective indicator.

 

(3) Digitalis poisoning reaction and treatment

The toxic reactions of digitalis preparations are as follows:

 

i. Gastrointestinal reactions: loss of appetite is the earliest symptom of poisoning, followed by nausea, vomiting, and occasional gastrointestinal bleeding.

 

ii. Symptoms of the nervous system, such as headache, fatigue, insomnia, depression, dizziness and hallucinations.

 

iii. Visual abnormalities: yellow vision, green vision, red vision, blurred vision, flashing, etc. may occur.

 

iv. Heart performance: Digitalis poisoning can induce arrhythmia and aggravation of heart failure.

Common arrhythmias are: ventricular premature beats, often in two, three or multiple sources. Paroxysmal atrial tachycardia with atrioventricular block. nonparoxysmal border tachycardia with or without accompanying AV block. ventricular tachycardia. Atrial fibrillation with high AV block. The above types can occur at the same time or in succession. Such arrhythmia is found to be a manifestation of drug poisoning when taking digitalis.

Electrocardiograms may show ST-T changes in fishhook-like or spoon-like shapes. These changes only reflect the effects of digitalis on the electrocardiogram and do not indicate digitalis poisoning. The direct effect of digitalis poisoning on the myocardium can cause focal myocardial degeneration or necrosis, thereby weakening myocardial contractility and aggravating heart failure.

 

The diagnosis of digitalis poisoning is mainly based on the patient’s sensitivity to digitalis. There were excessive doses of digitalis, factors that induce poisoning and symptoms of arrhythmia and electrocardiogram after administration.

Comprehensive analysis and diagnosis: The determination of serum digoxin concentration has certain reference value for the diagnosis of digitalis poisoning, but it also has limitation. For example, the effective blood concentration of digoxin is ≤1.92nmol / L (1.5ng / ml), and most of the poisoned persons are> 2.5. nmol / L (2ng / ml). But there are a few poisoned patients with serum digoxin concentration <1.92nmol / L (1.5ng / ml). So comprehensive analysis should be in combination with clinical manifestations.

 

1. The first step in the treatment of digitalis poisoning is to immediately stop digitalis.

At the same time, suspend diuretics. Give potassium supplements to those with hypokalemia. Patients with mild poisoning can recover within a few days after the above treatment. For severe arrhythmia, such as frequent, triple or triple ventricular premature beats, especially ventricular tachycardia, the following methods can be usable:

 

a. Potassium chloride 6-8g / day, divisible into doses. Or 1-2g of potassium chloride added to 500ml of 5% glucose solution, intravenous drip. Repeate administration if necessary. Oliguria, renal insufficiency and patients with high AV block are contraindicated.

 

b. For those who suffer from premature beats and tachycardia due to digitalis poisoning, phenytoin sodium, lidocaine, and propranolol can be usable. For usage, see the section “Arrhythmia”. Magnesium sulfate is effective for digitalis-induced arrhythmia.

Usage: 20% to 40ml of 25% magnesium sulfate solution and 250 to 500ml of polarized solution slowly drip into the vein. People with renal insufficiency should be used with caution. This medicine can inhibit atrioventricular conduction  and slow heart rate or blood pressure.

 

c. For arrhythmia, one can try atropine. Place those with high atrioventricular block accompanied by Ass syndrome with a temporary on-demand pacemaker.

 

d. Digitalis-specific antibodies for the treatment of various severe arrhythmias caused by digitalis poisoning have a rapid and specific effect, which is a new progress in the treatment of digitalis poisoning and is in trial.

 

2. Other cardiac glycosides stubborn spirits are oleander preparations

Tablets have similar effects to digoxin.

Oral dosage: effective therapeutic amount is 0.5-1.5mg and maintenance amount is 0.125-0.75mg per day.

 

3. Noncardiac glycoside

(1) Dopamine and dobutamine: Its main role is to directly excite the heart’s β-adrenergic receptors and enhance myocardial contractility and cardiac blood volume.

Usage: It is advisable to start infusion of dopamine at 2-5ug / kg per minute, and adjust it according to the condition later. If the dose is too large, the heart rate will increase, and the surrounding blood vessels will constrict and increase the load. Dobutamine started to be infused intravenously at a rate of 2.5 ug / kg per minute and gradually increased by 10 ug / kg. It has a strong positive muscular effect and few side effects.

 

(2) Phenoxybenzol is a β1 receptor stimulant which has the effect of strengthening myocardial contractility without contracting surrounding blood vessels or causing arrhythmia.

Usage: Generally 30-200mg / day orally, if necessary, 15ug / kg intravenous infusion per minute can be used. It is suitable for beta blockers and low-exhaustive heart failure that acute myocardial infarction causes.

 

(3) Pyridoxine acts on β receptors (β1β2) and excites them. In addition to enhancing myocardial contractility, it also has a strong role in dilating blood vessels and releasing airway obstruction.

Usage: 20mg 3-4 times.

Side effects: occasional nausea and anxiety.

 

(4) Aminopyridone hydrazone can strengthen myocardial contractility without blood pressure, heart rate or heart rhythm changes and the mechanism of action is unclear.

Usage: 300-900mg / day orally. This is effective for patients with refractory heart failure. Thrombocytopenia can complicate long-term use.

 

3. Other Treatments

a. Those who have difficulty breathing can be given oxygen.

 

b. Complications and their treatment: The common complications and treatment of heart failure are as follows:

(1) Respiratory tract infections are more common. Due to blood stasis in the lungs during heart failure, bronchitis and pneumonia are likely to be secondary to antibiotics.

 

(2) Thrombosis and embolism: Prolonged bed rest can lead to venous thrombosis of the lower extremities, which can cause pulmonary embolism after shedding. The clinical manifestations of pulmonary embolism are closely related to the size of the emboli. Small pulmonary embolism can be asymptomatic, and there can be manifestation of large pulmonary embolism as sudden shortness of breath, chest pain, palpitations, hemoptysis and decreased blood pressure.

At the same time, pulmonary arterial pressure increases and right heart failure worsens. Corresponding lungs are dull, respiratory sounds reduce with moist rales. Some patients have pleural friction or pleural effusion. Sclera may have yellow stains or short-term atrial fibrillation attacks. 12 to 36 hours or several days after the onset of the disease, triangular or circular density-dense shadows appear in the lower lung field. Huge pulmonary embolism can cause cardiogenic shock and sudden death within minutes. Patients with heart failure accompanied by atrial fibrillation are prone to thrombus in the atrium. The embolism may cause embolism of the brain, kidney, limbs or mesentery.

 

Patients who have been bedridden for a long time should pay attention to turning over and massaging their limbs for passive activities in time to prevent thrombosis. For those who have emboli to cause limb arterial embolism, treat mild patients with urokinase or streptokinase for thrombolytic therapy. Treat those with severe limb ischemia as Surgical treatment.

 

(3) Cardiogenic liver cirrhosis: Due to long-term right heart failure, chronic congestion and hypoxia in the liver, hepatocyte atrophy and connective tissue hyperplasia in the central lobules occurs. Portal hypertension occurs in the later stage which is manifested by a large amount of ascites, enlarged spleen and cirrhosis.

Treatment: After cardiac diuresis and other treatments, the ascites still does not diminish. Puncture those with a large amount of ascites affecting the cardiopulmonary function with a proper amount of fluid.

 

(4) Electrolyte disorders often occur during the treatment of heart failure, especially after repeated or long-term application of diuretics. Hypokalemia and salt-loss hyponatremia are the most common.

 

i. Mild hypokalemia is general weakness, severe arrhythmia may occur in severe cases, digitalis toxicity is often aggravated, potassium salts must be added in time, potassium chloride may be taken orally 3-6g / day in mild cases, potassium chloride may be used in severe cases Intravenous infusion of 1-1.5g dissolved in 500ml of 5% glucose solution can be repeated if necessary.

 

ii. Salting hyponatremia syndrome is caused by a large amount of diuresis and restriction of sodium salt intake, which mostly occurs after a large amount of diuresis. Symptoms are acute, with weakness, muscle twitching, thirst, and loss of appetite. Severe cases may have symptoms such as headache, irritability, unconsciousness, and even coma. Patients had dry skin, thin pulses, decreased urine output, and even reduced blood pressure. Laboratory tests: blood sodium, chloride, and carbon dioxide have low binding power, and increased hematocrit. Treatment should not be limited to table salt, and can be slowly infused with 100% -500ml of 3% sodium chloride solution.

 

Second, actively prevent the cause and inducement

After the onset of heart failure, can improve it if one uses drugs and surgery to treat the underlying cause. For example, anemia corrects anemia, antihypertensive treatment of hypertensive heart disease, thyroid function adjustment of hyperthyroid heart disease, heart valve disease and surgical treatment of congenital heart disease. Both are important methods to prevent the disease from developing to heart failure. Actively and effectively avoiding or controlling the causes of heart failure, such as acute infection with rheumatism, arrhythmia. Overwork can often reduce or prevent the occurrence of heart failure.

 

Treatment of refractory heart failure

Some patients with severe chronic heart failure cannot improve their heart failure status with various treatment measures including rest, diet, digitalis and diuretics, which is called refractory heart failure. For patients with refractory heart failure, rule out the common causes of refractory heart failure one by one:

i. Whether the diagnosis is correct or missing, such as occult hyperthyroidism and anemia.

ii. Pay attention to the existence of complications, such as pulmonary infection, subacute bacterial endocarditis, electrolyte disturbance and pulmonary embolism.

iii. Whether the digitalis dose is appropriate, insufficient or excessive doses can affect the efficacy.

iv. Whether the diuretic in use is appropriate

v. Whether there are negative contractile drugs such as propranolol, which can make heart failure worse.

vi. Whether the original heart disease, such as chronic valvular disease, congenital heart disease, is surgically treated in a timely manner. Lost surgery often develops into refractory heart failure. Whether electrolyte disorders are corrected.

 

Observe and analyze every patient with refractory heart failure in detail to find out the reasons that affect the efficacy and appropriate treatment measures may be taken to improve the heart failure.

 

Prognosis

It depends on the condition of the original heart disease, the degree of heart failure and the response to treatment.

  

Acute Heart Failure

Acute heart failure is the most common is acute pulmonary edema caused by acute left heart failure.

 

Etiology and Pathogenesis

I. Extensive acute myocardial infarction, acute myocarditis or aggressive hypertension. Left ventricular blood volume drops sharply, and pulmonary circulation pressure rises.

 

2. Mitral valve stenosis, especially with tachycardia, shortens the ventricular diastole, the blood in the left atrium cannot flow into the left ventricle sufficiently and the left atrium stasis dilates. This leads to increase in pulmonary venous pressure.

 

3. Severe arrhythmias, such as prolonged tachyarrhythmias or severe bradycardia, left ventricular filling and decreased blood output, leading to increased left atrium and pulmonary venous pressure.

 

4. The infusion is too fast or too much. The load of the heart suddenly increases in patients with original left heart failure and can cause acute pulmonary hypertension.

 

Due to the sudden increase in pulmonary vein and pulmonary capillary pressure caused by the above-mentioned causes, when the pulmonary capillary osmotic pressure exceeds 4.8kpa (36mmHg), a large amount of serous fluid leaks out from the capillaries into the pulmonary interstitial and alveoli. Acute lung Severe edema in the left ventricle causes a sharp decrease in blood output and cardiogenic shock.

 

Clinical manifestations of Acute Heart Failure

Patients often experience extreme difficulty breathing, forced to breathe, fear of expression, irritability, frequent coughing and a large amount of white or bloody foamy sputum. In severe cases, a large amount of foamy liquid can flow out of the nose lips pale, sweating, limbs damp and cold, both lungs covered with wet rales. Auscultation of the heart may have diastolic galloping rhythm, the pulse increases faster and may show alternating pulses. Blood pressure drops and severe patients may develop cardiogenic shock.

 

Diagnosis and Differential Diagnosis of Acute Heart afilure

The diagnosis is mainly on the basis of the above history and clinical manifestations. Differentiate the disease from bronchial asthma.

 

Treatment of Acute Heart Failure

 Acute pulmonary edema is a medical emergency. It s must to diagnose it promptly and rescue quickly.

 

1. Sedation: Inject subcutaneously or intramuscularly 5-10mg of morphine or 50-100mg of Dolentine to calm the patient. Expand peripheral blood vessels, reduce blood volume and reduce breathing difficulties. For the elderly, consciousness, respiratory depression, shock or combined pulmonary infection are contraindicated.

 

2. Oxygen inhalation and pressurization. High flow rate of oxygen is 6-8 liters per minute. One can inhale it through a nasal tube after flowing through 25-70% alcohol. Pressurization can reduce fluid leakage in the alveoli. Rupture to improve ventilation and use silicone defoamers to eliminate foam.

 

3. Reducing venous return: Patients should take a sitting or lying position with their legs drooping to reduce venous return. If necessary, a tourniquet can be added to the extremities and three limbs are ligated in turn. The limbs are changed every 5 minutes and the average is 15 minutes. Relax for 5 minutes to ensure that there is no affect on limb circulation.

 

4. Diuretic intravenous administration of fast and strong diuretics such as furosemide 20-40mg or sodium diuretic 25-40mg added to intravenous glucose injection to reduce blood volume, reduce heart load. Take it to prevent or correct a large number of diuretic accompanied onset of hypokalemia and hypovolemia.

 

5. Intravenous infusion of nitroprusside or phentolamine to reduce pulmonary circulation pressure, but vasodilators should be used to reduce hypotension. But one can also use it to reduce pulmonary circulation venous pressure by containing hypoglycerol or isosorbide dinitrate.

 

6. Cardiotonics such as those who have not used digitalis recently, can be injected intravenously with rapid-acting digitalis preparations, such as cedilan and poisonous trichoside K, etc., for pulmonary edema caused by mitral valve stenosis. In addition to atrial fibrillation, which is associated with a rapid ventricular rate, There is nee of no cardiotonic drugs to avoid increased pulmonary congestion due to increased right ventricular output.

 

7. Aminophylline can be used for those with bronchospasm. 0.25g of aminophylline is added to 20ml of 10% glucose solution and diluted slowly after intravenous injection, which can reduce bronchospasm, expand coronary arteries and strengthen diuresis.

Side effects: Premature ventricular contraction and / or ventricular tachycardia. Use it with caution.

 

8. The corticosteroid hydrocortisone 100-200mg or dexamethasone 10mg added to the glucose solution intravenously can also help control pulmonary edema.

 

9. The treatment of pre-existing diseases and predisposing factors: If there is a tachyarrhythmia, control it quickly.

 

 

 

See also:

 

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