El EEG fue normal y la polisomnografía nocturna mostró actividad irritativa y la clase funcional de angina y disnea en pacientes con angina refractaria y se .. paroxística frontal en 11 pacientes (% y temporal en 6 pacientes (%. Causas de epilepsia tardia em uma clínica de epilepsia do Estado de Santa. HEMOGLOBINURIA PAROXÍSTICA A FRIGORE. 13 OTRAS CAUSAS DE ANEMIA HEMOLÍTICA ADQUIRIDA Hemoglobinuria paroxística nocturna ( HPN) . y el enfermo presenta palidez de piel y mucosas, disnea, ansiedad e ictericia. tico diferencial con causas de citopenias y displasia 2) Estudio de hemoglobinuria paroxística nocturna. (HPN) Disnea de reposo.

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Los botones se encuentran debajo. There is no single definition of heart failure. This concept is ambiguous and incomplete, however, because heart failure is a composite of clinical symptoms, physical signs, and abnormalities on the hemodynamic, neurohormonal, biochemical, anatomic and cellular levels.

In addition, the actual cardiac output, venous return or absolute metabolic requirements are not usually measured in clinical practice. Heart failure is a syndrome characterized by symptoms and physical signs which are secondary to a change in function of the ventricles, caisas or load conditions. Clinical stages in the evolution of heart failure Heart failure is a continuous spectrum of changes, from the subtle loss of normal function to the presence of cusas refractory to medial therapy.

The patient with cardiomyopathy may maintain caisas normal ventricular function; the progression of dysfunction may be sudden or gradual.

Asymptomatic ventricular dysfunction is characterized by the absence of symptoms or decline in functional capacity, even in the absence of treatment. It may be associated with different changes causad cardiac physiology, including ventricular dilatation, regional wall motion abnormalities, and decreases in the LV ejection fraction and of other parameters of ventricular function.

In compensated heart failure the symptoms are controlled by medical therapy. In decompensated heart failure, praoxistica persist despite usual therapy and are refractory to adjustments in drugs and dosages. Determinants of ventricular function. Ventricular function, and cardiac function in general, depends upon the interaction of four factors that regulate the volume of blood expelled by the heart the cardiac output: The first three determine the volume of blood expelled with each beat the stroke or ejection volumewhile the heart rate affects the cardiac output by varying the number of contractions per unit time.

These four factors, which are intrinsic regulators of heart function, are all influenced by the nervous system. In the failing heart, especially in ischemic heart disease, it is also important to consider some purely mechanical factors, such as the synergy of ventricular contraction, the integrity of the septum, paroxistiva the competence of the atrioventricular valves.

Objectives The objectives of treatment of the patient with heart failure are many, but they may be summarized in two principles: Nevertheless, the rest of the listed objectives should not be forgotten, as medical therapy now has the potential for decreasing morbidity hospital admissions, embolism, etc.

Correction of aggravating factors Often a lack of response to conventional therapy for heart failure is due to the presence of uncorrected aggravating or precipitating factors. It is important to always consider the possibility of such factors, particularly in cases of refractory failure. Treatment of Heart Failure.

epilepsia temporal refractaria: Topics by

Drugs This is a simple and pragmatic classification of the vast numbers and types of medications in the pharmacopoeia for the treatment of heart failure. Theoretical hemodynamic effects of different drugs for heart failure Effects of different treatments on the relationship between ventricular filling pressure LVEDP and stroke volume.

Diuretics D and venous vasodilators V decrease the ventricular filling pressure in patients with heart failure and normal or elevated LVEDP, but except in patients with marked elevation of LVEDP, the stroke volume does not change. The pure arterial vasodilators A produce an increase in the stroke volume in patients with failure and an elevated LVEDP.

Inotropic drugs I increase the stroke volume with a lesser effect of the ventricular filling pressure.

Insuficiencia cardíaca congestiva

Effect of the principle pharmacologic patoxistica on the majority of symptoms, reduction in mortality, prevention of symptom development and control of neurohormonal abnormalities.

In the presence of symptoms of heart failure, diuretics or neurohormonal inhibitors should be added. The use of caudas remains controversial. Pxroxistica more advanced stages, in the presence of poorly controlled symptoms, newer drugs can be tried, reserving the inotropes for patients whose symptoms are uncontrollable with other medications.


In any case, secondary prevention and assisting the patients in adapting to their limitations should remain in mind. Classification and mechanisms of action Diuretics are drugs which eliminate Na and water by acting directly on the kidney. This category does not include other drugs with principle actions different from the diuretics, but which increase diuresis by improving heart failure or by mechanisms on the kidney which are incompletely understood.

The diuretics are the primary line of therapy for the majority of patients with heart failure and pulmonary congestion.


Diuretics loop, thiazides and potassium-sparing produce a net loss of Na and water acting directly on the kidney, decrease acute symptoms which result from fluid retention dyspnea, edema. Diuretic drugs are classically divided into three groups: Thiazide diuretics inhibit the active transport of Cl-Na in the cortical diluting segment of the ascending limb of the Loop of Henle. Loop diuretics inhibit the transport of Cl-Na-K in the thick portion of the ascending limb of the Loop of Henle.

Potassium-sparing diuretics inhibit the reabsorption of Na in the distal convoluted and collecting tubules. The act from the luminal surface inhibiting the active transport of Cl and the subsequent diffusion of Na and water in the cortical diluting segment of the ascending portion of the loop of Henle.

In addition they increase tubular reabsorption of uric acid, Ca and Mg. There are important differences in the strength and duration of diuretic action depending on which thiazide is used. By inhibiting carbonic anhydrase, they increase the urinary elimination of HCO Spironolactone is a competitive antagonist of aldosterone, interfering with its induction of synthesis of proteins which specifically facilitate Na reabsorption.

As a result, its diuretic action depends on the role that aldosterone plays in the retention of water and Na. Mechanisms of action Diuretics decrease volume and preload, and as a result are very effective at improving the signs of pulmonary and systemic venous congestion.

They do not change the cardiac output CObut CO may fall if an excessive decrease in preload occurs.

They slightly improve arterial distensibility, but this effect is of no clinical relevance. The main drawback to diuretics use is their effect on the neurohormonal milieu, increasing the plasma levels of noradrenaline NAangiotensin II Ang II and aldosterone, and the plasma renin activity PRA.

Adverse effects of thiazide and loop diuretics Thiazide and loop diuretics create electrolyte imbalances: They also create metabolic changes hyperglycemia, hyperuricemia, gout, increase in LDL-cholesterol and triglyceridesimpotence and menstrual cramps. Cutaneous allergic reactions rash, pruritis are frequent. In addition, these are cross-reactions between the various thiazides except chlorthalidone and because of their chemical resemblance, with furosemide and bumetanide.

Thiazides can aggravate myopia in pregnant women. Adverse effects of thiazide and loop diuretics Known adverse reactions include parenchymal pancreatitis, cholestatic jaundice, hemolytic anemia, thrombocytopeniagastrointestinal effects ethacrynic acidmyalgias bumetanide, piretanide and muscle cramps related to electrolyte disorders. Loop diuretics are associated with ototoxicity with loss of hearing and balance and these are more frequent in patients with renal insufficiency or with concomitant use of aminoglycoside antibiotics.

They may also cause interstitial nephritis. Rash, prurito Treatment of heart failure. Adverse reactions to potassium-sparing agents The main adverse reaction to these agents is hyperkalemia, which occurs mostly in patients with renal failure, particularly if they are also receiving ACE inhibitors.

They may also create metabolic acidosis, muscle cramps and weakness, and cutaneous allergic reactions.

It accumulates in skeletal muscle, liver and heart, where it may reach concentrations that cwusas 10 to 50 times higher than serum levels. This explains why hemodialysis eliminates little of the digoxin load in digoxin toxicity. Cardiac uptake of digoxin increases in patients with hypokalemia and decreases in the presence of hyperkalemia, hypercalcemia or hypomagnesemia. Digoxin undergoes very little biotransformation, and is mainly eliminated through glomerular filtration and somewhat by tubular secretion.

In patients with renal insufficiency, the half life of digoxin increases aproxistica, so that the maintenance dose must be determined according to the creatinine clearance, generally requiring half of the usual dose disnwa, in severe cases, intermittent dosing.

The time required to reach stable serum levels is 5 half-lives, that is, 7 days. Loading can be accomplished: This is not advisable except in cases of emergency, as it does paroxisgica allow individualization of the treatment and increases the risk of cardiac toxicity. In the majority of adults, the maintenance dose of digoxin is 0. Digoxin displaced the ventricular function curve up and to the left, meaning that it increases the cardiac output at any noctuurna pressure.


All of these effects explain when digoxin decreases the signs of congestion and peripheral hypoperfusion in the patient with heart failure. The increase in cardiac output reduces the heart rate, the peripheral vascular resistance, and offsets the increased myocardial demand for oxygen that the increase in contractility might create. Neurohormonal effects Digoxin, at the doses which augment cardiac contractility, restores the inhibitory effect of the arterial baroreceptors and markedly inhibits the activity of the sympathetic nervous system, which can be seen in the reduction of plasma levels of noradrenaline, the activity of peripheral sympathetic system, and the activity of the renin-angiotensin- aldosterone system RAAS.

This neurohormonal inhibition reduces the heart bocturna, the peripheral vascular resistance and the signs of congestion and peripheral hypoperfusion in the patient with heart failure. This creates the question paroxlstica what point do the beneficial effects of digoxin reflect its positive inotropic quality.

Digoxin also decreases noctuna reabsorption of Na and water; this natriuretic action, secondary to the increase in cardiac output, increases renal perfusion and the glomerular filtration rate, decreasing renal vasoconstriction and the activation of the RAAS.

After days of treatment, digoxin withdrawal produced a significant worsening in heart failure which was greater than that observed in the group of patients in whom digoxin was maintained.

N Causad J Med ; The patients were treated with digoxin or placebo, in addition to conventional therapy over a mean of 37 months months. No differences in mortality were observed between the two treatment groups.

There was no observed effect on survival, but it decreased slightly the number of admissions for cardiovascular causes and also increased the incidence of serious arrhythmias and episodes of acute myocardial infarction. The results of this study probably demand redefinition of the indication for the use of digoxin in patients with heart failure. Puede ser combinada con otras drogas Treatment of heart failure.

Noctura by diuretics and ACEI it is also useful in patients in sinus rhythm with systolic heart failure. It is also useful in patients who do not respond to diuretics and vasodilators and in severe heart failure associated with hypotension when vasodilators are contraindicated. Digoxin is more effective in heart failure with low cardiac output associated with cardiomyopathies, ischemic cardiomyopathy, arterial hypertension or causzs valvular disease with left ventricular failure.

The results of the study of survival with digoxin require a reassessment of the indications for digoxin use in patients with heart failure.

Probably digoxin will become a second-line drug, and its use may be restricted to patients with refractory symptoms, except in patient with rapid atrial fibrillation. Contraindications Vausas only absolute contraindication for digoxin use is the presence of digoxin toxicity.

paroxistic Digoxin toxicity Digoxin has a narrow therapeutic margin, and digoxin intoxication remains relatively frequent although it has diminished somewhat as it has become better recognized and lower doses pxroxistica being prescribed. Digoxin may cause any type of cardiac arrhythmia, although at times the ECG may be nonspecific. In addition, depression of sinoatrial node function dausas produce bradycardia and even complete sinoatrial block.

It prolongs the refractory period and depresses conduction velocity across the A-V node lengthens the PR interval on the ECGthereby creating different grade of conduction block, which may precede the appearance of reentrant nodal tachycardias and nodal rhythms.

Exacerbation of heart failure in patients treated with digoxin should raise the question of digoxin toxicity. Ginecomastia, galactorrea Treatment of heart failure. Digoxin paroxitica Extracardiac adverse reactions: Positive inotropic agents The use of inotropic agents in heart failure is intended to increase contractility and cardiac output to meet the metabolic needs of the body.

Theoretically, their use should be greatest in heart failure associated with a decrease in systolic function and marked cardiomegaly, depression of ejection fraction and elevated left ventricular filling pressure.

In addition to the cardiac glycosides, other positive inotropic agents include: