Acute Heart Failure

Image showing circulation cycle of blood from the heart, throughout body tissue, back to the heart and then the lungs.

The main function of the heart is to pump oxygenated blood from the heart, throughout the body, and return oxygen depleted blood to the lungs. This cycle takes only 13 seconds and is interrupted in acute heart failure.

The contraction of heart muscles, the resistance of blood vessels and valves all maintain the pressure and direction of flow to complete the circulation cycle.

Blood Pressure

Blood pressure is a measure of the force of blood as it is pushed through circulation. We measure 2 values:

Systolic Blood Pressure (SBP): force when the heart contracts

Diastolic Blood Pressure (DBP): force when the heart relaxes

Blood pressure is reported as SBP/DBP.

Pathophysiology

In heart failure the heart muscles become weak. They lose contractility and the walls of the heart start to stretch.

Think of the stretch in new knit sweater versus the looseness after it has been through the wash a few times.

The heart is not able to fill up with blood or contract normally. The overall result is less pressure and less volume of blood per pump. The circulation pathway is compromised.

B-type Natriuretic Peptide

When the heart muscle stretches it releases a hormone called proBNP. ProBNP immediately splits into B-type Natriuretic Peptide (BNP) and N-terminal pro-BNP (NT-proBNP).

BNP is biologically active. It attempts to compensate for heart failure by signaling blood vessels to dilate or widen. This will reduce the pressure in systemic circulation that the failing heart has to pump against.

BNP also stimulates the kidneys to increase sodium and water excretion. This will decrease the amount of blood returning to the heart (the preload), which takes some pressure off the weakened heart muscles.

Image showing stretched heart muscles in acute heart failure release proBNP. ProBNP then breaks sown into active BNP and NT-proBNP. BNP then causes vasodilation and increased excretion of sodium and water by the kidneys. This helps to compensate for the failing heart.

In acute heart failure, levels of BNP and NT-proBNP will rise significantly. The stretched heart muscles are releasing proBNP is large quantities so that blood vessels and the kidneys can try to compensate.

Both levels can be tested and used as a diagnostic criteria in combination with patient presentation for acute decompensated heart failure.

BNP levels in ADHF >100pg/dL

NT-proBNP levels in ADHF >300pg/dL

Impaired function can happen gradually over time (chronic heart failure) or suddenly (acute heart failure). This unit is focused on acute heart failure.

Compensation

The body will interpret decreases in pressure and output from the heart as low blood pressure. To correct this the kidneys will increase sodium and water retention to increase blood volume. This is the opposite of what BNP is asking the kidneys to do.

Image showing how the kidneys compensate in acute heart failure. As the outflow of blood from the heart into blood vessels decreases, the kidneys increase the amount of sodium and water it retains to increase the volume of plasma in blood vessels. This helps to maintain blood pressure.

The blood vessels will also constrict in an attempt to increase pressure and facilitate tissue perfusion. This is the opposite of what BNP is asking the vessels to do.

Illustration showing how blood vessels compensate in acute heart failure. As the volume of blood pumped out by the heart decreases, blood vessels will constrict to increase pressure. This will help to maintain the pressure needed to get blood to distant tissues.

This compensation unfortunately makes it even more difficult for an already failing heart. It now has to pump against even higher resistance from the vessels.

Image showing the opposing compensations that happen in heart failure. Stretch heart muscles release a hormone BNP that tries to relieve pressure on the by reducing blood volume and increasing vasodilation. While the kidneys sense low blood pressure and do the exact opposite.

In heart failure, the body is essentially fighting against itself.

This a very delicate balance of compensation triggered by BNP release and opposing compensation triggered by hypoperfusion.

When balance can be maintained a patient will be in compensated heart failure.

Tipping the balance can trigger acute decompensated heart failure.

Acute decompensated heart failure (ADHF) occurs when:

1. hypoperfusion compensation can no longer keep up with decreased cardiac output and BNP compensation causing hypoperfusion of tissues and organs

2. renal compensation triggering increased sodium and fluid retention outweighs BNP compensation leading to fluid congestion

Hypoperfusion

Hypoperfusion is the result of reduced cardiac output coupled with BNP’s triggering of vasodilation and reduced blood volume. Every organ in the body will be affected by hypoperfusion.

It reduces oxygen and nutrient availability. Signs and symptoms of patients presenting with hypoperfusion include:

Illustration of the different organs that are affected by hypoperfusion in heart failure. It includes the heart at the center surrounded by the intestines, the brain, the extremities, the liver and the kidenys.

Altered alertness and cognition from decreased cerebral perfusion

Cold extremities from decreased perfusion to distant tissues

Accumulation of metabolic waste from decreased perfusion to kidneys and liver

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Cardiac Output

Cardiac output can be measured as an estimation of hypoperfusion. It is the amount of blood pumped by the heart each minute.

Normal cardiac output is 4-7 L/min. In acute heart failure it can be 2-4 L/min. Typically a cardiac output of ~2.2L/min or lower indicated significant hypoperfusion.

Cold and Warm

Not all patients with acute decompensated heart failure will have low cardiac output.

If they do we describe them as cold. If they are perfusing normally, we described them as warm.

Congestion

Congestion in acute decompensated heart failure is the result of fluid accumulation. This occurs from the kidneys attempt to restore blood pressure by retaining sodium and water.

The heart muscle may also be too weak to accept venous return from systemic circulation so plasma pools in the venous system. Like hypoperfusion, fluid congestion has systemic implications.

As excess fluid accumulates it infiltrates organs and other body tissues. Signs and symptoms of patients presenting with congestion in ADHF include:

Illustration showing how fluid accumulation in heart failure affects different parts of the body. It shows swollen legs for edema, fluid filled lungs for shortness of breath, man sitting in chair for orthopnea.
It shows a fluid filled abdomen for ascites. A swollen liver for hepatomegaly. A swollen neck for jugular distention and a swollen spleen for splenomegaly.

Swelling in the extremities (hands, arms, feet, ankles, legs) as fluid seeps into those tissues. This is known as edema.

Shortness of breath with activity and/ or at rest as fluid accumulates in the lungs. On examination, we hear rales (a rattling or bubbling sounds in the lungs).

Difficulty breathing when lying down. This is known as orthopnea.

Fluid accumulation can occur in the abdomen causing ascites, in the liver causing hepatomegaly and in the spleen causing splenomegaly.

A classic sign of increased fluid accumulation in the atria is jugular vein distention. The neck vein will visibly protrude.

Pulmonary Capillary Wedge Pressure

Fluid congestion in ADHF is measured by the pulmonary capillary wedge pressure (PCWP). A device is placed into the heart where it measures the pressure in the left atrium.

Normal PCWP is 8-12 mmHg. In ADHF it is 18-30mmHg.

Measuring PCWP is considered an invasive procedure. In practice it is not routinely performed. We rely on the symptoms we just discussed as markers of fluid overload.

Wet and Dry

Not all patients with ADHF will have fluid congestion.

If they do we describe them as wet. If they are euvolemic, we described them as dry.

4 Subsets of ADHF

When a patient presents with acute decompensated heart failure, we categorize them based on the absence or presence of hypoperfusion and the absence or presence of congestion. This creates 4 categories of ADHF.

I. Warm & Dry

These patients have adequate perfusion and no fluid accumulation. They are in ADHF heart failure which is identified by an elevated BNP or NT-proBNP but their body is able to balance BNP compensation and hypoperfusion compensation.

II. Warm & Wet

These patients have adequate perfusion but have signs and symptoms of fluid accumulation like edema, orthopnea. Hypoperfusion compensation outweighs BNP compensation at the kidneys.

III. Cold & Dry

These patients have low perfusion but so symptoms of fluid accumulation.

IV. Cold & Wet

These patients have low perfusion and fluid accumulation.

Illustration showing the 4 categories of acute decompensated heart failure based on symptoms of fluid congestion and hypoperfusion. It has 4 quadrants. Upper left shows warm and dry. Upper right shows warm and wet. Bottom left shows cold and dry. Botom right shows cold and wet.

Treatment

Management of ADHF is determined by which of those 4 categories best represents the patient.

We use intravenous diuretics to alleviate fluid congestion.

Intravenous vasodilators reduce the preload and systemic vascular resistance.

Ionotropes are used to increase the contractility of the heart when systolic blood pressure falls below 90mmHg.

Final Thoughts

With the information in this unit, you have a great foundation to delve into and really understand the AHA/ACC/HFSA Heart Failure Guidelines. Check out our other units in cariology:

Acute Coronary Syndrome: What You Need to Know

Atrial Fibrillation: Where to Start

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The information on this website is intended to be used solely for educational and informational purposes. While the content may be about specific medical and health care issues, it is not a substitute for or replacement of personalized medical advice and is not intended to be used as the sole basis for making individualized medical or health-related decisions.