Lectures on heart failure treatment

2021-01-30 12:00 AM

Symptoms of decreased cardiac output: fatigue, poor exercise tolerance, decreased peripheral perfusion, severe heart failure, decreased vital organ perfusion; Decreased renal perfusion, reduced cerebral perfusion ultimately leads to dizziness.


Heart failure is the heart's inability to maintain an adequate supply of the heart to meet the body's metabolic needs.

Based on the pathophysiology and the difference of treatment methods people distinguish.

Acute heart failure: acute pulmonary edema, cardiogenic shock, acute decompensated heart failure.

Chronic heart failure:

Systolic dysfunction occurs when the heart's ability to eject blood (ejection fraction (EF) decreases).

Diastolic dysfunction occurs when ventricular elasticity decreases, resulting in poor blood reception.

Clinical manifestations

Symptoms of decreased cardiac output: fatigue, poor exercise tolerance, decreased peripheral perfusion, severe heart failure, decreased vital organ perfusion; Decreased renal perfusion, reduced cerebral perfusion ultimately leads to dizziness.

Symptoms of pulmonary and systemic venous congestion: dyspnea while lying down, dyspnea during exertion, paroxysmal nocturnal dyspnea, peripheral edema, venous distention, pleural effusion, pericardium, blood stasis in the liver, ascites.

In young children (1 year old) and neonates the clinical manifestations of heart failure differ from those of adults and adults, the manifestations are usually: the child refuses to suckle, does not gain weight and develops, has rapid breathing, excessive sweating If the left atrium is too large, it can compress the left lung bronchus and collapse the lungs, children often get lung infections. On physical examination, the liver is enlarged, usually edema in the face, rarely swelling of the limbs or ascites, and often cold in hands and feet.



Can see enlarged heart, pulmonary congestion, pleural effusion.


Depending on the cause, an ECG does not help assess heart function.


Measure the size of the heart chambers, survey heart valve condition, regional disorders and evaluate left ventricular function reduced fractional rate <45 - 50% in cases of apparent left ventricular systolic failure.

BNP (brain sodiumuretic peptide)

Pre pro-BNP is formed in the ventricles, including 2 components N-terminal-pro-BNP (NT-pro-BNP) and BNP. These hormones are highly reliable and specialized in the diagnosis and elimination of heart failure. BNP is especially valuable in helping the stool of cardiac dyspnea with dyspnea due to lung diseases, especially useful in emergency resuscitation.

Other tests

Depending on the cause.


Diagnosis determined: Based on the standard Framingham

 Framingham's diagnostic criteria for congestive heart failure

Main standard

Secondary standard

Great difficulty breathing at night

Floating neck veins

Rales in the lungs

Big heart

Pulmonary edema

Horse riding T3

Increased venous pressure (> 16cmH2O)

Feedback of venous venous liver (+)

Phu chi

Cough at night

Difficulty breathing with exertion

Big liver

Pleural effusion

Living capacity decreased by 1/3 compared to normal

Fast heart (> 120 / min)

Primary or secondary

Weight loss ³ 4.5kg in 5 days of treatment

A clinical diagnosis of congestive heart failure occurs when ³ one primary criterion and two sub-criteria exist.

Treatment of heart failure

The principles of treatment

It is necessary to identify patients with heart failure (differentiated from other conditions with symptoms resembling heart failure) and the degree of heart failure.

Find and treat underlying disease.

Find and address the motivating factors.    

Specialized treatment of heart failure (for degree of congestive heart failure).

Purpose of treatment

Preventing disease progression.

Improve quality of life.

Extend the life of the patient.

Treatment goals

Control water retention and sodium salt.

Increases the force of heart muscle contraction.

Reduced cardiac work.

Reduces pulmonary and systemic venous congestion.

Specific treatment

Depends on each specific individual, based on severity, cause, comorbidities, motivating factors.

Do not take medicine:

Reduced work on the heart:

Limiting body activity: reducing cardiac work, reducing myocardial oxygen consumption, reducing the body's requirement for stroke volume, cardiac output, cardiac index, decreased arterial blood pressure, increased urine output. Reasonable rest depending on the degree of heart failure, avoiding the risk of venous thrombosis: from limited activity to absolute bed rest, passive and active limb is recommended.

Eat a light snack each time, eat a few times.

Weight loss in obese patients reduces peripheral resistance and the need for O2.

Keep it quiet.

Stop smoking, avoid alcohol.

Common reliever: benzodiazepam, or the use of Morphine in severe and acute cases.

Limit salt (2g / day):

Water restriction: (<1.5l / day) important for patients with hyponatremia (<130mmol / l) and volume overload, if serum sodium <125mmol / l can cause arrhythmia

Oxygen for severe dyspnea:

Purple green, decrease O2, decrease Pa O2.

Helps patients reduce difficulty breathing, reduce pulmonary vascular spasm.

Dialysis or ultrafiltration:

 In patients with severe heart and renal impairment, poor responses to water restriction and diuretics were observed.

Other mechanical measures:

Purging, extracting blood, rotating chi syrup: Avoid taking large amounts of fluid quickly and causing hypotension.

Specialized drug treatment

General principles:

Drug treatment includes vasodilators, controlling salt and water retention, increasing left ventricular contractility. Vasodilators are the cornerstone of treatment in patients with heart failure.


Vasodilators can reduce pre-load or post-load, or both.

Varicose veins will mainly reduce the preload, reduce left ventricular filling pressure and reduce pulmonary congestion.

Arterial dilators reduce afterload by decreasing peripheral resistance thereby increasing the minute cardiac output, reducing left ventricular filling pressure and reducing myocardial wall tension. Patients with open heart valves, severe heart failure with increased peripheral resistance or heart failure combined with hypertension are most beneficial when using artery-reducing agents to reduce the after-load.


Hypotension, orthostatic hypotension, and pre-renal hyperuremia may occur with vasodilators (arterial or venous) in patients with low or normal ventricular filling pressure.

Use caution when using vasodilators in patients with:

Fixed cardiac flow (aortic stenosis, aortic stenosis).

Diastolic dysfunction (restrictive cardiomyopathy)

Oral vasodilators:

ACE inhibitors:

Reduce sudden death, improve exertion ability.

The artery-dilating effect is equivalent to that of a varicose.

ACE inhibitors reduce left ventricular filling pressure and decrease peripheral resistance thereby increasing cardiac output without altering heart rate, without drug resistance. Therefore, all patients with heart failure due to left ventricular dysfunction should be on ACE inhibitors for long-term treatment, unless they are intolerant or have contraindications.

It is recommended to start with a test dose (test dose should be given in the evening) then gradually increase the dose up

Side effects:

Renal failure in patients with bilateral renal artery stenosis.

Rash, allergic edema.

Loss of taste.

Primary protein.

Lower blood pressure.

Increased blood potassium.


Therefore, it is necessary to monitor renal function, analyze urine and count granulocytes during long-term treatment with ACE inhibitors.


Severe renal impairment: serum creatinine> 500mmol / l.

Increased blood potassium.

Reduce the volume of circulation.

Reduces blood sodium.

Aortic stenosis.

Pregnancy, lactation.

Angiotensin II receptor antagonists inhibit the Renin Angiotensin system by specifically inhibiting Angiotensin II receptors, thus not increasing bradykinin levels (Bradykinin causes side effects: cough, angioedema, renal failure, hypotension. ). This drug can be used in lieu of an ACE inhibitor (in a patient with an ACE inhibitor intolerance) or with an ACE inhibitor. Adverse events and adverse events were similar to ACE inhibitors except for cough.

Angiotensin II converting enzyme inhibitors and receptor antagonists and dosage:

Drug name


Initial dose

Maximum dose / day

Number of times / day

ACE inhibitors


Lopril 12,5; 25; 50 mg



3- 4


Renitec 2.5; 5; ten; 20mg





Zestril 5; ten; 20mg





Accupril, Accutel 5; 20mg





Coversyl 2; 4mg





Triatec 1.25; 2.5mg




Angiotensin II receptor antagonism


Tozaar 25; 50mg





Diovan, Tareg, valzaar 40; 80; 160mg





Approvel 75; 150; 300mg





Micardis 40; 80mg





Varicose veins mainly thereby reduce the symptoms of congestion in the lungs and veins, reduce myocardial anemia by reducing ventricular filling pressure and direct dilatation of coronary arteries.

 Nitrate-free (12 hours) space is required to avoid drug resistance:

Drug name

Way for


Starting t / d

Long lasting effect


DL seal

0.3 - 0.6mg

30 seconds

15 - 30 minutes


(Lenitral 2.6mg)

To drink

2.5 - 6.6mg

1 hour

2 - 4 hours




2.5 - 5cm

10 - 60cm

1 hour

6 - 24 hours

Isosorbid dinitrate

(Risordan, ISDN)

To drink

10 - 60mg

30 minutes

4 - 6 hours

Isosorbid mononitrate

(ISMN 40; 60mg,

Imdur 30; 60mg)

To drink

10 - 40 -60mg

30 minutes

8 - 21 hours

Side effects:

Postural hypotension.

Headache, flushing.

The heart is reflexive.


Direct circuit expansion and reduce afterload.

Very effective in patients with mitral regurgitation or aortic regurgitation.

The drug causes reflex tachycardia and increases myocardial oxygen consumption. Therefore, it should be used with caution in patients with coronary artery disease.

In addition drugs also cause lupus erythematosus-like syndrome.

Usual dose: 25 - 100mg, used 3-4 times a day.

Calcium inhibitors:

Varicose arteries more than veins.

Advantages of calcium inhibitors:

Reducing myocardial anemia.

Reduce the after-load.

Diastolic relaxation of the heart muscle.

Diltiazem and Verapamil should not be used in the treatment of heart failure.

Dihydropyridine group calcium inhibitors are not indicated for heart failure except for heart failure due to hypertension or myocardial anemia.


Arterial and venous dilatation through the a1-inhibitory effect is now rarely used because it is easily resistant to the drug and does not prolong the patient's life.

Parenteral vasodilators:

Use only in patients with severe heart failure or in patients who are unable to drink should start with low dose and before termination need to reduce the dose slowly.


The effect of varicose veins is more than that used in heart failure due to acute myocardial infarction or unstable angina.

Initial dose 10microgram / min intravenous infusion.

The maximum dose should not exceed 300microgram / minute.

Resistance occurs early, so try to switch to oral or patchy skin.

Half-life 1- 3 minutes.

The dose should not be increased when the systolic BP is below 100mmHg.

Sodium Nitroprusside:

The effect of dilating the arteries rather than the varicose veins is more effective in treating heart failure caused by high blood pressure or by an open valve mechanism.


In combination with the reduction of water salts, diuretics were formerly the basic primary treatment for heart failure, diuretics are used when there are signs of fluid retention.

When using high doses, should not lose> 0.5 - 1 kg of weight / day.

Monitor sodium and potassium lowering by electrolyte.

Monitor urea, blood creatinine.

The three main groups of diuretics used in the treatment of heart failure are: thiazide group, loop diuretic and potassium-sparing diuretic (see dosage and effects table).


Digitalis may improve symptoms and quality of life in heart failure patients, but not on disease progression.

Mechanism of action:

Inhibition of ATPase Na + K + enzyme effect in myocardial membrane means sodium pump inhibition, so more sodium in cells, accompanied by increased Ca ++ in cells leads to increased myocardial contractility.

Activation of the parasympathetic system: sinus node slowdown, atrioventricular node suppression, anorexia, nausea, vomiting.


Mild spasm of peripheral arteries and veins => coronary spasm.

Increase the phase 4 slope thereby increasing the automation of the peripheral drives.

Conduction increases in the Kent bundle in WPW syndrome.


Heart failure with atrial fibrillation.

Heart failure with left ventricular contraction function decreased EF <30% and sinus rhythm: galloping horse, wet rales 2 lungs.

Some ventricular arrhythmias.


Obstructive hypertrophic cardiomyopathy (unless atrial fibrillation is present).

Digoxin poisoning.

Progressive Grade I, II, and III AV block (if pacemaker is not present).

Left ventricular diastolic dysfunction with normal or increased EF.

Sinus node failure syndrome.

Chronic cardiopulmonary heart (unless atrial fibrillation is rapid ventricular response).

Severe renal failure.

Severe ventricular arrhythmias.

Before fibrillation (avoid ventricular arrhythmias after fibrillation).

Digoxin sensitivity.

Several conditions increase susceptibility to digoxin:

> 70 years old.

Reduces blood potassium.

Increased blood potassium.

Lack of O2.


Acute myocardial infarction.

Reduced blood Magnesium.

Increased blood calcium.

Reduced blood calcium.



Powder contamination.

Drugs that increase the concentration of digoxin in serum:

Quinidine (decreased renal clearance).



Digoxin dose should be reduced by half when used with these drugs

Digoxin dose should be increased when used with the following drugs:









Drug name

Gastrointestinal absorption

Start working

T / 2

Elimination (metabolic)

Load dose (mg)

Maintenance dose


55- 75%

15-30 minutes

36- 48 hours

Kidneys and a little in the gastrointestinal tract

- U: 1,25-1,5

0.25 x2 / day

x2 days

- TM:, 75- 1





4-6 days


- U: 0.7-1.2

0.3 / day x

3 days

- TM: 1mg



No load dose is required when treating chronic heart failure conditions.

Evaluation of renal function and plasma potassium should be assessed prior to initiation of treatment.

If maintenance dose 0.25mg / day should have 1-2 days a week without drugs.

In elderly patients should be maintained with a dose of 0.125mg / day.

Digitalis poisoning:

Extra-cardiac symptoms:

Gastrointestinal disturbances: anorexia, nausea, diarrhea, weight loss.

CNS symptoms: visual hallucinations, mental confusion, insomnia, weakness, greenish-yellow vision, blurred vision, spots.

Heart symptoms: much more important because it can cause sudden death. All types of arrhythmias can be found in digitalis poisoning. The most common arrhythmias due to digitalis poisoning are:

Ventricular extrasystole went to double, multifocal rhythm

Atrioventricular block:

Grade I and II atrioventricular block.

Atrial tachycardia with block changes.

Grade III atrioventricular block.

Atrial fibrillation with a slow, steady ventricular response (<50 / p).

Fast heart beat:

Non-paroxysmal junction tachycardia with atrioventricular dissociation or augmented junction rhythm.

Ventricular tachycardia and ventricular fibrillation.

Slow tempo:

Sinus slowdown.

Sinus arrest, atrial sinus block.


If heart failure worsens despite sufficient digoxin doses should be suspected digoxin poisoning.

Carotid sinus massage can cause ventricular fibrillation and asystole in digitalis poisoning patients

Management of digitalis poisoning:

General measures:

Stop digoxin for at least 3 days.

Stop the diuretic, if necessary use a potassium-sparing diuretic.

Quantification of serum digoxin.

Check dosage and find and adjust for digoxin sensitizers.

Record ECG, if arrhythmia is observed with Monitor.

Special treatment when needed:

Severe heart failure.

Arrhythmia is life-threatening.

Tachycardia: ventricular tachycardia, atrial tachycardia with block, multifocal ventricular extrasystole.

Give potassium provided that serum potassium is not increased, renal failure and atrioventricular block are absent:

In mild case: drink 40-80mEq (2.5-5g KCL).

For severe cases: 40- 60mEq / 1 liter of 9% natriclorur (or 5% dextrose intravenously for> 4 hours or 30-40 mEq / 20- 50ml 9% NaCl 9% o via electric syring at the rate of 0.5- 1mEq / p.

Lidocaine effectively treats both ventricular and external multi-focal ventricles quickly. Direct intravenous injection 1- 1.5mg / kg and drip infusion 2-3mg / min

Phenytoin; effective in the treatment of ventricular arrhythmias due to digitalis poisoning but should be saved when lidocaine and potassium are ineffective:

Drink 100 - 150mg / 6 - 8 hours.

Intravenous: 250mg diluted in 9% o NaCl at the rate of 25-50mg / min by central vein, can be repeated after 20 minutes.

Attention: Lower blood pressure, dizziness, asystole, ventricular fibrillation may occur, especially if the rate of phenytoin infusion increases.

Beta blocker: used in the absence of response to the above drugs, effective in ventricular ectopic or supraventricular without atrioventricular block

Bradycardia: bradycardia that causes fainting or worsening hemodynamics:

Atropin: 0.4-0.6mg intravenously until the maximum dose is 2mg.

Do not use sympathomimetic drugs.

Pacemaker is temporary if it does not respond to Atropin.

Electric shock is very dangerous, only used in life-threatening cases where other methods fail, so it starts with low energy.

Fab antibody fragment in the treatment of patient's life-threatening arrhythmias, conventional measures are ineffective and especially when blood potassium is high.

Activated charcoal 50 - 100g increases the change of digoxin through the digestive tract.

The drugs that increase myocardial contractility have sympathomimetic activity:

Dopamine and dobutamin are often used in series (2-4 days) in either inert heart failure or severe acute heart failure

Beta inhibitors:

Beta-blockers inhibit the activation of beta-adrenergic receptors; Inhibits the harmful effects of prolonged sympathetic stimulation. Beta-blockers have been shown to provide symptom relief and improve clinical status and prolong the life of patients with heart failure.

These benefits were observed with carvedilol, metoprolol and bisoprolol in patients on ACE inhibitors because of their combined inhibitory effect on the humoral nervous system. Therefore, all patients with moderate to severe stable heart failure (grade II-IV NYHA) due to left ventricular systolic dysfunction should use one of these beta-blockers for long-term treatment unless contraindicated. .

Drug name


Initial dose

Maximum dose / day

Number of times / day


Betabloc, 25; 50 mg

12.5mg (5mg)




Concor 5; 10mg





Dilatrend, talliton, cardivas 6,25; 12.5mg




Putting tools to support synchronous contraction of the ventricles, heart transplant ...

Evaluate the effectiveness of treatment

Body weight: fast, morning weight allows to evaluate the effectiveness of diuretic treatment.

Keep heart rate 70-80 / min at rest (count full-minute heart rate if patient has atrial fibrillation).

Significant physical signs: level of carotid venous stasis, degree of edema, liver size, moist rales in the lungs, gallop.

Diuresis: diuresis results are a useful guide to treatment efficacy.

Chest radiograph: smaller heart size (cardiopulmonary index), decreased pulmonary congestion are signs of improvement.

Some treatments according to the cause

Heart failure due to diastolic dysfunction

It is necessary to find and treat the causes of diastolic heart failure: coronary heart disease, hypertension, myocardial hypertrophy and spasmodic pericarditis.

Regulates tachycardia and restores sinus rhythm when possible.   

A beta blocker, a calcium inhibitor (verapamil) that can slow heart rate and increase diastolic time may be tried.

Diuretics should be careful not to reduce the pre-load.

ACE inhibitors can improve left ventricular dilatation and long term reduce left ventricular hypertrophy.

Digitalis is a contraindication.

Stenosis of the mitral valve

Addresses factors that reduce diastolic time (thereby increasing left atrial pressure): fever, tachycardia, exertion.

Diuretics: decreased pulmonary edema and congestion, nitrate reduces pre-load thereby reducing pulmonary congestion.

Long-term anticoagulant in atrial fibrillation, sinus rhythm but left atrium> 60mm, history of embolism or thrombosis on cardiac ECHO.

Digitalis: reduce ventricular rate in the presence of atrial fibrillation with rapid ventricular response, can be combined with low dose beta or diltiazem inhibitors so that heart rate is 60-70 / p at rest.

New atrial fibrillation: defibrillation with electric shock or with drugs (Amiodarone or quinidine). Need to use anticoagulants 3 weeks before and after the change of rhythm.

Prevention of infectious endocarditis: body hygiene, procedures, minor surgery or tooth extraction, dental treatment.

Prevent recurrence low in young patients.

Surgical treatment of mitral stenosis.

Aortic valve stenosis

Avoid strenuous physical activity.

Digoxin is only used when left ventricular dilatation and systolic function impairment.

Be careful when using diuretics because it causes a decrease in circulating volume leading to a decrease in cardiac output: use a low dose when the patient has oedema.

Do not use or only use low doses of nitrate and other vasodilators.

Prophylaxis of infectious endocarditis.

The best practice is still surgical treatment: aortic valve replacement.

Two-leaf valve opening

The basic treatment is surgery to repair or replace the mitral valve.

Disease without heart failure: do not need to use medicine to treat heart failure, just limit exercise and prevent infectious endocarditis.

Symptoms of heart failure:


Other ACE inhibitors or vasodilators.

Digoxin if not responding to treatment with the above 2 drugs.

Anticoagulant (see mitral stenosis).

Aortic valve opening

The basic treatment is surgery; repair or replace the valve. Surgery is required before severe left ventricular function is reduced (<40%).

Medical treatments include:

Limit your movement.

Limit salt and water.


Vasodilation: ACE inhibitors should be used.


Find and treat the cause and the triggers.

Prophylaxis of infectious endocarditis.