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.

CO

Stroke volume (SV) is the volume of blood ejected from the heart with each contraction (normally ranges from 60 ml to 130 ml). CO (CO) is the volume of blood ejected by each ventricle per minute (normally ranges from 4 liters/minute to 8 liters/minute in resting adults). CO can be calculated using the formula, SV x heart rate = CO. An adequate CO is essential to supply oxygen and nutrients to major organs and peripheral tissues. For example, a reduction in CO 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 CO. Cardiac index better assesses whether the patient’s CO is adequate because it is adjusted for the patient’s body size. To calculate cardiac index, divide the patient’s CO by his or her body surface area. Normal cardiac index for adults ranges from 2.5 L/minute/m2 to 4.2 L/minute/m2.

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 and snap like a rubber band to send blood on its way. However, a point can be reached 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 CO 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 CO 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 CO. 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 mechanism.

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 CO 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 CO.

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 capillary.

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 (NTG), 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 CO. 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, and raises CO (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 CO. 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 dysrhythmias, 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, tachypnea, 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), NTG, 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 or her 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.

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 heart’s workload 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 he or she 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 ischemia.

Nesiritide, a human B-type natriuretic peptide, administered by an IV bolus followed by an infusion, is indicated strictly 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 infusion dose may be increased by 0.005 mcg/kg/min, no more frequently than every three hours up to a maximum dose of 0.03 mcg/kg/min. The dose-limiting effect of nesiritide is hypotension; therefore blood pressure must be monitored closely during therapy. Moreover, recent studies show that the drug may worsen renal function and mortality. The risks and availability of other therapy to relieve heart failure should be evaluated before initiating nesiritide therapy.

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 CO, 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, as well as 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 ventricular rhythm disturbances. Serum electrolytes and renal function should also be monitored because milrinone improves CO, 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 tubules. 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 postacute 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.

A ventricular assist device (VAD) can also be inserted to help reduce preload and afterload in a failing heart. The device, typically attached to the left ventricle and aorta, assists in pumping blood throughout the body. VADs are designed to reduce the heart’s workload and increase CO in patients with ventricular failure who are awaiting cardiac transplantation. A complete list of devices is available at the American Heart Association website .

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 miniature 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.