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Hemodynamics For the Bedside Nurse
Authors: Jennifer D. Hebra, RN, MSN, MBA & Laura Hackler, RN, CCRN, CEN

Course Objectives

The goal of this program is to update nurses’ knowledge about hemodynamics and appropriate
therapeutic interventions for preload and afterload. After completion of this session, the participant will
be able to —

• Define preload and afterload.

• Identify two factors each that can affect preload and afterload.
• List two therapeutic interventions each for preload and afterload problems.

Concepts of “preload” and “afterload” can overload busy medical-surgical nurses who now care for
patients with cardiovascular problems that would have landed them in critical care beds just a few years
ago. Because of the complexity of these patients’ diseases, sophisticated hemodynamic assessment is
no longer reserved exclusively for critical care practitioners. Nurses in step-down, medical-surgical,
and even home care settings need a basic understanding of hemodynamic concepts to guide their day-
to-day practice.

Hemodynamics refers to the forces, such as preload and afterload that affect circulating blood
throughout the body. Nurses assess the stability of these forces when they take a blood pressure or
palpate a pulse. Although the interaction of these forces is quite complex, the concepts can be more
easily comprehended by substituting the word, “stretch” for preload, and “resistance” for afterload.
Preload and afterload are closely related and reflect the heart’s effectiveness in managing blood flow in
and out of its chambers.

Cardiac Output

Stroke volume (SV) is the volume of blood ejected from the heart with each contraction (normally
ranges from 60 ml to 130 ml). Cardiac output (CO) is the volume of blood ejected by each ventricle per
minute (normally ranges 4 liters/minute to 8 liters/minute in resting adults). Cardiac output can be
calculated using the formula, SV x heart rate = CO. An adequate cardiac output is essential to supply
oxygen and nutrients to major organs and peripheral tissues. For example, a reduction in cardiac output
may diminish blood flow to the brain and result in an altered level of consciousness and impaired
cognition. Changes in heart rate, contractility (force and velocity of heart muscle fiber contraction),
preload, or afterload can all affect cardiac output.

Understanding Preload

Preload is the force that stretches the muscle fibers of a resting heart — how much they are stretched
just before contraction. Preload is also defined as all the factors that affect wall tension at the end of
diastole. The amount of blood present within the atria and ventricles before contraction and the
condition of the myocardium determine the stretch or preload of the heart muscle. The greater the
volume of blood in a heart chamber, the greater the preload. As the blood volume in the left ventricle
increases, the cardiac muscle stretches and, up to a point, ejects its volume more effectively. Ideally, an
adequately filled and stretched left ventricle should briskly contract, snap like a rubber band, to send
blood on its way. However, there is also a point at which this stretch is so extreme that output is
diminished. The relationship between fiber stretch and contractile force is known as “Frank-Starling’s
Law of the Heart.”

Starling’s Law states that, up to a point, the more a cardiac muscle is stretched in diastole (resting
stage), the more forcefully it contracts in the next systole (ejection stage). Optimal cardiac output is
dependent upon blood volume, heart rate, and achieving the appropriate amount of stretch. For
example, a hemorrhaging trauma victim may have a ventricle that is inadequately filled. Therefore
cardiac output is reduced because of two mechanisms: inadequate blood volume in the ventricle and a
lesser force of contraction that is caused by less muscle fiber stretch. However, compensatory
mechanisms are triggered by the sympathetic nervous system in response to shock — an increased
heart rate and contractility as well as other mechanisms temporarily sustain cardiac output. Replacing
lost circulating volume supports these compensatory mechanisms by increasing preload, thus
enhancing cardiac muscle stretch and subsequent contraction, optimizing the effect of the Starling

For the patient in heart failure who is volume overloaded, the ventricle has the opposite problem.
Increased ventricular volume raises pressure within the ventricles, thereby augmenting myocardial
stretch or preload and subsequent contraction. Initially, this serves as a compensatory mechanism with
cardiac function reaching the maximum beneficial stretch described in Starling’s Law, thus cardiac
output is optimized. If fluid overload continues, the pressure within the ventricle rises beyond the point
of beneficial stretch leading to less effective cardiac contraction (the stretched rubber band without the
snap), and decreasing cardiac output.

Right ventricular preload — the central venous pressure (CVP) or right atrial pressure (RAP) — can be
measured by a catheter placed in the right atrium. However, clinicians usually focus on preload of the
left ventricle (LV), which is the largest and last chamber to eject blood to most of the body. A
pulmonary artery catheter, also know as a Swan-Ganz catheter, when inserted into the pulmonary artery
and wedged in a pulmonary capillary, indirectly measures LV preload, better known as left ventricular
end-diastolic pressure (LVEDP). End-diastole represents the moment in the cardiac contraction-
relaxation cycle when the ventricle contains the greatest volume of blood, just before it contracts and
ejects its volume. The volume and the stretch or amount of tension placed on the heart muscle at that
point determines the pressure. The wedged pulmonary artery catheter reflects LVEDP because at end-
diastole, the mitral valve is open and this creates communication between the left atria, left ventricle,
and pulmonary vascular bed. In other words, “the doors are all open” from the LV to the pulmonary

Several factors influence preload, including the distribution of blood within the body, total blood
volume, sympathetic stimulation, the presence and force of atrial contraction, called the “atrial kick,”
and natriuretic peptides.

Blood distribution refers to the allocation of blood within the body (and in this case, the ventricles) at
any specific time. The venous system can be thought of as a large reservoir that can hold blood in the
peripheral circulation or return it back to the heart, depending on the state of vasodilation or
vasoconstriction. For example, a drug that dilates the venous system, such as nitroglycerin, reduces
preload by causing a greater volume of the blood to remain in peripheral circulation. Conversely, when
higher blood pressure is needed, sympathetic stimulation causes vasoconstriction, which increases
peripheral blood return to the central circulation augmenting cardiac output. Gravity affects this
distribution of blood. For example, elevating the legs of a supine patient redistributes blood to core
organs such as the heart and brain, when blood pressure is low. This position increases venous return
by adding to the volume in the left ventricle, which stretches the cardiac muscle and enhances preload,
raises cardiac output, and potentially, blood pressure.

When too much blood is distributed to a diseased left ventricle with poor muscle tone, it may become
overstretched. This condition is known as left ventricular failure. In left ventricular failure, ventricular
contraction is not forceful enough to eject its volume of blood with each contraction. A nurse can help
patients with left ventricular failure by using gravity to redistribute blood to the lower extremities. The
nurse can do this by encouraging patients to dangle their legs from the side of the bed. Reducing
venous return in this way lessens preload and decreases the work of the heart. Many patients with heart
failure, who develop lung congestion caused by increased preload, learn this principle on their own.
They find that sleeping in a recliner, elevating the head of the bed, or resting on multiple pillows
alleviates symptoms and allows them to breathe easier. They are able to breathe easier because blood
is redistributed, decreasing the volume that the heart must handle as preload.

Total blood volume is the common pool of blood available for distribution throughout the body. Too
little or too much can adversely affect preload. For example, blood loss from trauma may reduce
preload by having less blood available to stretch the ventricle. Thus, a simple fluid bolus often
improves the patient’s cardiac status. On the other hand, a patient may have more blood in the body
than the heart can handle causing the ventricle to overstretch, as happens with heart failure.
Administering a diuretic can reduce the volume and lessen preload so the heart doesn’t have to work so
hard. Years ago, one treatment for fluid overload associated with heart failure was to therapeutically
phlebotomize or “bleed” a patient to lessen the volume stretching the myocardium by decreasing total
blood volume.

Sympathetic stimulation can enhance preload by causing blood vessels to constrict, which increases
blood return to the left ventricle. This stimulation also increases heart rate, ultimately improving
cardiac output. However, if the myocardium is injured, a faster heart rate can overwork the heart and
increase its oxygen demand causing further myocardial ischemia and injury.

Atrial contraction occurs just before the valves between the atria and ventricles close and is commonly
referred to as “atrial kick.” This action enhances ventricular preload by contributing up to 30% more
volume to the ventricles at the end of diastole. When dysrrhythmias, such as atrial fibrillation occur and
normal atrial contraction is absent, this added volume is lost.

When atrial and ventricular chamber pressures increase, endogenous peptides, called atrial natriuretic
peptides (ANP) and B-type natriuretic peptides (BNP) are released to reduce preload and afterload.
These peptides cause selective vasodilation and decrease sodium reabsoption, thereby decreasing
preload and afterload.

Interventions for Preload Problems

Signs of volume overload — dyspnea, the presence of crackles or possibly wheezes on auscultation,
pulmonary edema, jugular vein distention, and pitting edema of the ankles — may indicate a problem
with increased preload. Medical interventions usually include a drug regimen of first line drugs —
morphine, furosemide (Lasix), nitroglycerin, and if necessary second line drugs such as dopamine,
dobutamine, and nesiritide (Natrecor).

Morphine, in addition to relieving pain and anxiety, dilates peripheral vessels. This action redistributes
blood, which “pools” in dependent areas, such as the legs, especially if the patient also dangles his legs
or has the head of the bed elevated. Pooling decreases the volume returned to the heart, which
subsequently reduces the volume that a failing ventricle must manage. If the failing left ventricle
ineffectively empties its contents, it accepts less blood from the pulmonary circulation, causing blood
to pool in the lungs which can lead to pulmonary edema. The dose of morphine, usually ranges from 2
mg to 10 mg IV, titrated according to the patient’s response. Some patients may experience
hypotension due to arterial as well as venous dilation with small doses, while others may require
repeated high doses to achieve a therapeutic effect. Blood pressure must be monitored frequently in
these patients.

Furosemide is an effective diuretic that diminishes total blood volume by boosting urine output, as long
as the heart works well enough to adequately perfuse functioning kidneys. The initial recommended
dose is 0.5 mg/kg to 1.0 mg/kg by slow IV injection. Typically IV doses range from 20 mg to 40 mg,
although a dose of 100 mg may be necessary in an emergency situation. Blood pressure needs careful
monitoring when IV diuretics are administered, particularly if the patient is already hypotensive.
Additional medications may be necessary to support blood pressure during diuresis. Electrolyte
monitoring is also critical because reduced levels of serum magnesium and potassium may cause lethal
heart rhythm disturbances.

Nitroglycerin (NTG), like morphine, produces venous dilation, redistributing blood volume to the
peripheral circulation and pooling blood away from the heart. NTG is also effective in relieving cardiac
chest pain because it lessens the workload of the heart and reduces cardiac muscle oxygen
requirements. Additionally, higher doses of IV NTG enhance oxygen delivery by improving circulation
through the coronary arteries. Sublingual NTG, which is mainly a venodilator, reduces preload in
patients who take it to treat angina, whereas IV NTG given in higher doses causes arterial dilation,
thereby reducing ischemia.

Dopamine, a precursor of norepinephrine, is administered as a continuous infusion. It affects preload

by causing vasoconstriction or dilation through its effect on the sympathetic nervous system. The
effects of dopamine are dose-dependent. When administered at a low dose of 2 mcg/kg/min to 4
mcg/kg/min, it has peripheral vasodilating effects but causes little or no increase in renal perfusion or
force of myocardial contraction (positive inotropy) as previously thought. It may work by promoting
diuresis, which decreases preload, as would its vasodilating effect. Dopamine administered at this dose
range has no direct effect on blood pressure. Therefore if the patient begins demonstrating blood
pressure fluctuations , look for other causes, such as vascular volume depletion, anxiety, or pain.

Moderate-range doses between 5 mcg/kg/min and 10 mcg/kg/min directly improve preload by causing
venous constriction and increasing myocardial contractility through sympathetic stimulation.
Dopamine is considered a second-line treatment for pulmonary edema when the patient’s systolic blood
pressure ranges between 70 mmHg and 100 mmHg and is exhibiting signs and symptoms of shock.
Systemic and splanchnic (gut) vasoconstriction occurs when doses exceed 10 mcg/kg/ min. A word of
caution: the risk of myocardial and peripheral ischemia, is greater as the dose increases. The need for
supplemental oxygen should be evaluated, chest pain should be treated promptly, and peripheral
perfusion indicators such as pulses and urine output should also be closely monitored. Tachycardia is
an adverse effect associated with dopamine administration and for a patient who has coronary heart
disease, the combination of increased contractility and tachycardia may significantly worsen ischemia.

Dobutamine, a synthetic catecholamine administered as a continuous IV infusion, is indicated for the

treatment of acute pulmonary edema when systolic blood pressure is greater than 100 mmHg, and no
signs of shock are present. It’s also indicated for severe systolic heart failure. Its effects are dose
dependent. Dobutamine increases myocardial contractility and heart rate, decreases LV preload, and
indirectly causes peripheral vasodilatation further reducing preload It is usually administered at doses
ranging from 5 to 20 mcg/kg/min; doses exceeding 20 mcg/kg/min increase the risk for myocardial

Nesiritide , a human B-type natriuretic peptide, administered by an IV bolus, followed by an infusion,

is indicated for acutely decompensated heart failure in patients who have dyspnea at rest or with
minimal activity. The drug binds to receptors on vascular smooth muscle and endothelial cells causing
smooth muscle relaxation. This relaxation causes vasodilation and consequently dose-dependent
reductions in pulmonary artery wedge pressure. The drug may also increase vascular permeability and
may reduce intravascular volume by causing diuresis.

The recommended dose of nesiritide is an IV bolus of 2 mcg/kg, followed by a continuous infusion of

0.01 mcg/kg/min. The dose-limiting effect of nesiritide is hypotension. The infusion dose may be
increased by 0.005 mcg/kg/min, no more frequently than every 3 hours up to a maximum dose of 0.03

Fundamentals of Afterload

Afterload is the resistance to ventricular ejection. Afterload is also defined as all the factors that
influence ventricular wall tension during systolic ejection. Sources of resistance include blood pressure,
systemic vascular resistance (SVR), and the condition of the aortic valve. When arterial
vasoconstriction raises SVR, as in shock, or the aortic valve is very tight or stiff, as in aortic stenosis,
the ventricle must generate a tremendous amount of pressure — or afterload — to overcome that
resistance. It’s like opening a door against a strong wind — it takes a lot of energy.

Sympathetic stimulation causes vasoconstriction of certain arteries, arterioles, and veins, thereby
raising blood pressure. This increases cardiac workload. The ventricle now has to generate enough
tension to raise the pressure within the ventricle above the pressure in the aorta to force the aortic valve
open. Only then can the ventricle eject its contents. Imagine that you have a 60cc syringe with a 25-
gauge needle on the end and you are trying to eject the contents of the syringe as quickly as possible. It
takes a tremendous amount of force to empty the contents of the syringe because the small diameter of
the needle acts as resistance to flow.

Aortic stenosis can be congenital or occur after infections such as rheumatic fever, or with aging as
calcium deposits on valve leaflets. All of these conditions have the effect of creating an obstruction to
the outflow of blood from the left ventricle. Consider the energy required to open a window that has
been painted shut versus a window that freely opens. Valves open because the pressure generated on
one side of the valve (left ventricle) exceeds the pressure on the other side (aorta). A stenotic valve
creates a great deal of resistance to ejection causing afterload to rise dramatically.

To open the aortic valve and eject blood, the ventricle has to overcome the resistance of the arterial
blood pressure and resistance caused by the valve. Therefore, patients with chronic, untreated
hypertension or aortic stenosis develop left ventricular hypertrophy in response to the high afterload.
The same phenomenon occurs in skeletal muscles when a person undertakes a weight-lifting program.

Interventions That Affect Afterload

Medications, technology, and independent nursing actions can be used to manipulate afterload.

Nitroprusside, a potent vasodilator, diminishes both systemic vascular resistance and venous return. Its
net effect is a reduction in preload and afterload resulting in a decreased work of the heart, improved
cardiac output, and relief of pulmonary congestion. It’s indicated for severe heart failure and
hypertensive emergencies. The recommended dose ranges from 0.1 mcg/kg/min to 5 mcg/kg/min as a
continuous IV infusion; doses up to 10 mcg/kg/min may be necessary. The IV solution container must
be wrapped in foil because exposure to light decomposes the drug. Cyanide toxicity is a risk for
patients with hepatic or renal insufficiency and those requiring doses of more than 3 mcg/kg/min of
nitroprusside for longer than 72 hours.

Milrinone (Primacor), a positive inotrope and vasodilator is indicated for the short-term IV treatment of
patients with acute symptomatic heart failure. Continuous BP monitoring is required. Milrinone is
administered as a loading dose of 50 mcg/kg given by slow IV push over 10 minutes. The loading dose
is followed by a continuous infusion of 0.375 mcg/kg/min, which may be increased to a maximum dose
of 0.75 mcg/kg/min and should not exceed 1.13 mg/kg/day. The infusion rate should be titrated
according to the patient’s hemodynamic and clinical response. Milrinone has not been shown to be safe
or effective if used for longer than 48 hours. Blood pressure and continuous cardiac monitoring should
be instituted during infusion because milrinone can cause hypotension and lethal cardiac rhythm
disturbances. Serum electrolytes should also be monitored because milrinone improves cardiac output
causing diuresis, which may lead to electrolyte imbalances.

Angiotensin converting enzyme (ACE) inhibitors, such as captopril (Capoten) and enalapril (Vasotec),
block the conversion of angiotensin I to angiotensin II. A potent vasoconstrictor, angiotensin II
stimulates the release of aldosterone, a hormone that regulates fluid balance. When circulating
angiotensin II is reduced systemic vascular resistance, or afterload, is also reduced. In addition preload
is reduced because less plasma aldosterone is available causing less sodium and water reabsorption by
the renal tubles. Patients taking ACE inhibitors should be monitored for hypotension, decreased serum
sodium levels, and elevated blood urea nitrogen (BUN) level. ACE inhibitors are indicated for
hypertension and post-acute myocardial infarction.

The intraaortic balloon pump (IABP) consists of an elongated balloon mounted on a catheter that is
inserted into the descending thoracic aorta, usually through the femoral artery. The device senses
systole and diastole, usually via the patient’s ECG signal. The balloon inflates at the onset of diastole,
raising aortic diastolic pressure. The coronary arteries fill almost exclusively during diastole, so raising
this pressure causes the coronary arteries to be perfused at a higher pressure, thereby enhancing
coronary artery blood flow. This treatment can be extremely helpful to a patient who has cardiac
ischemia. A competent aortic valve prevents blood from flowing back into the aorta. Therefore, severe
aortic regurgitation prohibits the use of this device.

The major effect of the IABP is afterload reduction. As the device senses the onset of systole, it quickly
deflates the balloon, causing an abrupt decrease in the pressure within the aorta. Recall that the aortic
valve opens because the ventricle generates greater pressure during systole than exists in the aorta.
When the balloon deflates at the beginning of systole and the pressure falls, the resistance to ejection
falls decreasing afterload. The ventricle can easily eject its contents against less resistance. This makes
the IABP a lifesaving device for many patients whose hearts cannot handle the normal workload, such
as patients with heart failure following cardiac surgery or those awaiting cardiac transplantation.

Nurses can also reduce afterload by helping patients reduce anxiety by maintaining a calm atmosphere
and controlling care when possible, and by providing measures to control pain. In our technologically
advanced world, we sometimes forget how much these factors influence patient outcomes. A patient
with myocardial damage will greatly benefit from nursing interventions that minimize cardiac
workload and oxygen demand by decreasing sympathetic stimulation.

Current research in maximizing the effectiveness of preload and afterload, also known as cardiac
unloading is exciting and progressive. This research includes continued use of the IABP, the possible
use of a minature intracardiac assist device, better understanding of neurohumoral activation and
compensatory immunologic responses, and pharmacologic therapies.

Concepts of preload and afterload are the foundations for learning and understanding complex
physiological changes and treatment options for managing cardiovascular disease. Nurses applying this
knowledge can coordinate medical and nursing interventions to promote better patient outcomes.

Jennifer D. Hebra, RN, MSN, MBA, formerly director, cardiovascular nursing, HeartCare Center,
Roper CareAlliance, Charleston, NC and currently a surgical nurse in St. Petersburg, FL.

Laura Hackler, RN, CCRN, CEN, is a critical care staff nurse, relief administrative supervisor, and
staff development educator at JFK Medical Center, Atlantis, FL.