In Heart Failure we could have; Congestion, Hypo perfusion, Hypotension. With combination of these findings I will create some patterns and then I will write some diagrams to simplify approach of HF. I put the easier one for treatment at the first and most difficult is the last one;

1- Congestion without hypo perfusion 2- Hypo perfusion without congestion 3- Congestion and hypotension

1- Congestion without hypo perfusion

The basic treatment of congestion is Vasodilator + Diuretic. But you should choose an approach according to etiology of congestion. There are three basic etiology of congestion:

The basic treatment of congestion is Vasodilator + Diuretic. But you should choose an approach according to etiology of congestion. There are three basic etiology of congestion:

A)  Pulmonary congestion due to left side Failure → The most important drug is high dose Vasodilator → the second important drug is Diuretic

B)  Edema, ascites, elevated JVP (or right side failure) → The most important drug; High dose Diuretic

C)  If systolic function ok → Diastolic failure → Decrease of pulse rate is important → use of diuretic with caution

You can understand this approach by thinking about these basics questions.

A) Why is vasodilator more important than diuretic in left side failure with pulmonary congestion?
Usually there is systolic dysfunction in left side failure and cardiac output decreases. By vasodilator we can decrease the afterload and increase cardiac output. Because when afterload decreases it will be easier for heart to pump the blood and left ventricular end diastolic pressure will decrease and pulmonary congestion will go away.
Also when you administer a loop diuretic to the patient the LVEDP will decrease and pulmonary congestion will go away. But if you administer a big dose of a loop diuretic to the patient, probably LVEDP will drop too much and according to Frank-Starling law cardiac output will decrease which is not a favorable effect in LV-failure!
See the graph of relationship between cardiac output and LVEDP.

B) Why is diuretic more important than vasodilator in peripheral edema and right side failure?
Congestive heart failure (CHF) is one of the most common chronic conditions. The most frequent presenting symptom for patients with CHF is dyspnea, which is often attributed to pulmonary edema and occurs in 93% of patients. The second most frequent symptom is peripheral edema, occurring in 70%. Naturally, one of the mainstays of therapy has been to target hypervolemia through the use of diuretics.
Briefly, when LVEDP is high due to hypervolemia, naturally the therapy has been to target hypervolemia through the use of diuretics. But when LVEDP is high because of left ventricular dysfunction and decrease of cardiac output, the therapy has been to target afterload by vasodilator to increase the cardiac output.


The graph of relationship between cardiac output and LVEDP
C1) Why should we use diuretic with caution in diastolic failure?
Cardiac output in the graph is the area of square. In both systolic and diastolic heart failure, LVEDP will increase and cardiac output will decrease. But the way of changes is so different.
The use of diuretics should be cautious. Because most appropriate LVEDP in these patients is very narrow range and excessive reduce of LVEDP by high-dose diuretic, lowers blood pressure and can worsen the symptoms of disease.

C2) Why is decrease of pulse rate important in diastolic failure?
In diastolic heart failure the volume of blood contained in the ventricles during diastole is lower than it should be, so Beta-blockers are the first-line therapy as they induce bradycardia and give time for ventricles to fill and increase cardiac output.
SHF = Systolic heart failure, DHF = Diastolic heart failure, ESP = End systolic pressure

2- Hypo perfusion without significant congestion

Usually because of infarction, cardiac output has decreased. By dropping afterload we can increase cardiac output. We can stimulate beta2 receptors which cause vasodilation (hence the decreased SVR). This is a great property for patients who need a decrease in their afterload, but can be problematic if they are hypovolemic and blood pressure will drop.

When there is not congestion, diuretic is not a good choice. Because there is not hypervolemia and LVEDP is high due to decreased cardiac output. So if you decrease LVEDP by diuretic without hypervolemia, LVEDP will drop too much and according to Frank-Starling law cardiac output will decrease which is not a favorable effect in systolic dysfunction. But usually small dose of diuretic is safe and permitted in this situation, if patient is not dehydrated and blood pressure is good. See the graph of relationship between cardiac output and LVEDP.

In this category we have two situation; A) No hypotension B) With hypotension;

A) No Hypotention, Cold peripheral → Hydration - Levosimendan (or use of Nitrate with caution) → If because of decreased cardiac output acute heart failure continues → Dobutamin

B1) Hypotention → Hydration → Use of Dobutamine with caution → If blood pressure drops → Noradrenaline

B2) Right ventricular infarctions → Hypotention → Hydration → If bradycardia then pacing support → Noradrenalin or Dobutamin

Some points on drugs

1- Levosimendan is a positive inotropic drug with vasodilator effects.

2- Dobutamine is a beta1 and beta2 agonist. So along with the positive inotropy/chronotropy/dromotropy that you get with the beta 1, you also stimulate beta2 receptors which cause vasodilation (hence the decreased SVR) This is a great property for patients who need a decrease in their afterload, but can be problematic if they are hypovolemic. Dobutamine, on the other hand, has alpha properties as well. So you will see vasoconstriction and an increase in SVR.

3- Noradrenaline is also useful in the treatment of right ventricular failure which follows a condition of acute pulmonary hypertension, because the improvement of cardiac performance established without adverse effects on the pulmonary pressures whose values on the contrary progressively declined.

 

3- Congestion and hypotension

Congestion with hypotension is a challenge in CCU. In this condition at first you should stabilize hemodynamic. So at first you should not administer any drug which could cause hemodynamic to worsen.

Hydration with caution → Dobutamine → If hypotension then Noradrenaline with caution → If pulmonary edema then CPAP → If blood pressure has stabilized → Diuretic infusion, started with low dose → Levosimendan in need → If hemodynamic has not stabilized → indication for heart transplantation? LVAD?

CPAP= continuous positive airway pressure, LVAD= left ventricular assist device

 

By Dr. Samad Ali Moradi, According to author's work experience and guidelines. The graph of relationship between cardiac output and LVEDP is from Duodecim Finnish cardiology reference book