Aortic valve stenosis
Aortic valve stenosis (AS) is a heart condition caused by the incomplete opening of the aortic valve.
The aortic valve controls the direction of blood flow from the left ventricle to the aorta. When in good working order, the aortic valve does not impede the flow of blood between these two spaces. Under some circumstances, the aortic valve becomes narrower than normal, impeding the flow of blood. This is known as aortic valve stenosis, or aortic stenosis, often abbreviated as AS.
Contents
1 Pathophysiology
2 Etiology
3 Prevalence
4 Physical examination
5 The electrocardiogram (ECG) in aortic stenosis
6 Major complications of aortic stenosis
6.1 Congestive heart failure
6.2 Syncope
6.3 Angina
7 Associated symptoms
8 Cautions
9 Calculation of valve area
9.1 Planimetry
9.2 The continuity equation
9.3 The Gorlin equation
9.4 The Hakki equation
10 References
Thursday, January 11, 2007
Frank-Starling law of the heart
Frank-Starling law of the heart
The Frank-Starling law of the heart (also known as Starling's law or the Frank-Starling mechanism) states that the more the ventricle is filled with blood during diastole (end-diastolic volume), the greater the volume of ejected blood will be during the resulting systolic contraction (stroke volume).
Effectively, this means that the force of contraction will increase as the heart is filled with more blood and is a direct consequence of the effect of an increasing load on a single muscle fibre. The force that any single muscle fibre generates is proportional to the initial sarcomere length (known as preload), and the stretch on the individual fibres is related to the end-diastolic volume of the ventricle. In the human heart, maximal force is generated with an initial sarcomere length of 2.2 micrometres, a length which is rarely exceeded in the normal heart.
This can be seen most dramatically in the case of a premature ventricular contraction. The premature ventricular contraction causes early emptying of the left ventricle (LV) into the aorta. Since the next ventricular contraction will come at its regular time, the filling time for the LV increases, causing an increased LV end diastolic volume. Because of the Frank-Starling law, the next ventricular contraction will be more forceful, causing the ejection of the larger than normal volume of blood, and bringing the LV end-systolic volume back to baseline.
For example, during venoconstriction the end diastolic volume increases, increasing preload, this will increase stroke volume. The heart will pump what it receives.
The above is true of healthy myocardium. In the failing heart, the more the myocardium is dilated, the weaker it can pump, as it then reverts to Laplace's law.
History
The law is named after the two physiologists, Otto Frank and Ernest Starling who first described it.
Long before the development of the sliding filament hypothesis and our understanding that active tension depends on the sarcomere's length, in 1914 Ernest Starling hypothesized that "the mechanical energy set free in the passage from the resting to the active state is a function of the length of the fiber." Therefore, the initial length of myocardial fibers determines the work done during the cardiac cycle.
See also
Starling equation
The Frank-Starling law of the heart (also known as Starling's law or the Frank-Starling mechanism) states that the more the ventricle is filled with blood during diastole (end-diastolic volume), the greater the volume of ejected blood will be during the resulting systolic contraction (stroke volume).
Effectively, this means that the force of contraction will increase as the heart is filled with more blood and is a direct consequence of the effect of an increasing load on a single muscle fibre. The force that any single muscle fibre generates is proportional to the initial sarcomere length (known as preload), and the stretch on the individual fibres is related to the end-diastolic volume of the ventricle. In the human heart, maximal force is generated with an initial sarcomere length of 2.2 micrometres, a length which is rarely exceeded in the normal heart.
This can be seen most dramatically in the case of a premature ventricular contraction. The premature ventricular contraction causes early emptying of the left ventricle (LV) into the aorta. Since the next ventricular contraction will come at its regular time, the filling time for the LV increases, causing an increased LV end diastolic volume. Because of the Frank-Starling law, the next ventricular contraction will be more forceful, causing the ejection of the larger than normal volume of blood, and bringing the LV end-systolic volume back to baseline.
For example, during venoconstriction the end diastolic volume increases, increasing preload, this will increase stroke volume. The heart will pump what it receives.
The above is true of healthy myocardium. In the failing heart, the more the myocardium is dilated, the weaker it can pump, as it then reverts to Laplace's law.
History
The law is named after the two physiologists, Otto Frank and Ernest Starling who first described it.
Long before the development of the sliding filament hypothesis and our understanding that active tension depends on the sarcomere's length, in 1914 Ernest Starling hypothesized that "the mechanical energy set free in the passage from the resting to the active state is a function of the length of the fiber." Therefore, the initial length of myocardial fibers determines the work done during the cardiac cycle.
See also
Starling equation
Cardiac output
Cardiac output
From Wikipedia, the free encyclopedia
Cardiac output is the volume of blood being pumped by the heart, in particular a ventricle in a minute. It is equal to the heart rate multiplied by the stroke volume.
Therefore, if there are 70 beats per minute, and 70 ml blood is ejected with each beat of the heart, the cardiac output is 4900 ml/minute. This value is typical for an average adult at rest, although cardiac output may reach up to 30 liters/minute during extreme exercise.
When cardiac output increases in a healthy but untrained individual, most of the increase can be attributed to increase in heart rate. Change of posture, increased sympathetic nervous system activity, and decreased parasympathetic nervous system activity can also increase cardiac output. Heart rate can vary by a factor of approximately 3, between 60 and 180 beats per minute, whilst stroke volume can vary between 70 and 120 ml, a factor of only 1.7.
Contents
1 Measuring Cardiac Output
1.1 The Fick Principle
1.2 Dilution methods
1.3 Doppler method
1.4 Pulmonary Artery Thermodilution (Trans-right-heart Thermodilution)
1.5 PulseCO and PiCCO Technology
1.6 FloTrac technology
1.7 Impedance plethysmography
2 Equations
//
Measuring Cardiac Output
There are many invasive and several non-invasive methods for measuring cardiac output in mammals.
A non-invasive method, often used in teaching students of physiology, reasons as follows:
The pressure in the heart rises as blood is forced into the aorta
The more stretched the aorta, the greater the pulse pressure
In healthy young subjects, each additional 2ml of blood results in a 1 mmHg rise in pressure
Therefore Stroke volume = 2ml x Pulse pressure
Cardiac Output is therefore 2ml x Pulse Pressure x Heart Rate
The Fick Principle
Fick principle involves measuring:
VO2 consumption per minute using a spirometer (with the subject re-breathing air) and a CO2 absorber
the oxygen content of blood taken from the pulmonary artery (representing venous blood)
the oxygen content of blood from a cannula in a peripheral artery (representing arterial blood)
From these values, we know that:
where CO = Cardiac Output, CA = Oxygen concentration of arterial blood and CV = Oxygen concentration of venous blood.
This allows us to say
and therefore calculate cardiac output.
Dilution methods
This method measures how fast flowing blood can dilute an indicator substance introduced to the circulatory system, usually using a pulmonary artery catheter. Early methods used a dye, the cardiac output being inversely proportional to the concentration of dye sampled downstream. More specifically, the cardiac output is equal to the quantity of indicator dye injected divided by the area under the dilution curve measured downstream (the Stewart-Hamilton equation):
The trapezoid rule is often used as an approximation of this integral. A more modern technique is to use cold saline as the indicator, and then measure the change in temperature downstream. Cardiac output can be affected by the phase of respiration, especially under mechanical ventilation, and should therefore be measured at a defined phase of the respiratory cycle (typically end-expiratory).
Doppler method
This technique uses ultrasound and the Doppler effect to measure cardiac output. The blood velocity through the aorta cause a 'Doppler shift' in the frequency of the returning ultrasound waves. Echocardiographic measurement of the aortic root cross-sectional area (or, alternatively, the descending aorta area) multiplied by the measured velocity time integral of flow through that area and heart rate, yields the cardiac output.
Pulmonary Artery Thermodilution (Trans-right-heart Thermodilution)
The pulmonary artery catheter (PAC) also known as the Swan-Ganz thermodilution catheter provides right heart blood pressures. Using the PAC thermodilution cardiac output can be measured. Modern catheters are fitted with a distal heated filament, which allows automatic thermodilution measurement via heating the blood and measuring the resultant thermodilution trace. This provides near continuous cardiac output monitoring. The PAC is used in assessment of haemodynamic status and direct intracardiac and pulmonary artery pressures. The distal (pulmonary artery) port allows sampling of mixed venous blood for the assessment of oxygen transport and the calculation of derived parameters such as oxygen consumption, oxygen utilization coefficient, and intrapulmonary shunt fraction.
The PAC is balloon tipped which can be inflated to occlude the pulmonary artery, the subsequence back pressure is a reflection of the left atrial filling pressure and until recently was considered a good indicator of preload.
The pulmonary artery wedge pressure (PAWP) has been superseded by more reliable techniques such as intrathoracic blood volume or stroke volume variation as indicators of volume status. The PAC also allows sampling of mixed venous blood, the oxygen content of which can be used to indicate the adequacy of overall oxygen delivery. The PAC has fallen out of common use as clinicians favour less invasive, less hazardous technologies for monitoring haemodynamic status. Considerable controversy exists over whether the PAC increases mortality; recent studies suggest it neither increases nor improves mortality. Complications such as cardiac tamponade, pulmonary artery rupture and air emboli are a danger.
PulseCO and PiCCO Technology
PiCCO (PULSION Medical Systems AG, Munich, Germany) and PulseCO (LiDCO Ltd, London, England) generate continuous cardiac output by analysis of the arterial blood pressure waveform. In both cases, an independent technique is required to provide initial calibration of the continuous cardiac output analysis, as arterial waveform analysis cannot account for unmeasured variables such as compliance of the vascular tree.
In the case of PiCCO, transpulmonary thermodilution is used as the independent technique. This uses the Stewart-Hamilton principle outlined above, but measured from central venous line to a central (i.e. femoral or axillary) arterial line. The cardiac output derived from this cold-saline thermodilution is used to calibrate the arterial pulse contour analysis, which can then provide continuous cardiac output monitoring. The PiCCO algorithm is dependent on blood pressure waveform morphology (i.e. mathematical analysis of the pulse contour waveform) and calculates continuous cardiac output as described by Wesseling and co-workers. Transpulmonary thermodilution spans right heart, pulmonary circulation and left heart; this allows further mathematical analysis of the thermodilution curve, giving measurements of cardiac filling volumes (GEDV), intrathoracic blood volume, and extravascular lung water.
In the case of LiDCO, the independent calibration technique is lithium dilution, again using the Stewart-Hamilton principle. Lithium dilution has the advantage of being usable from a peripheral vein to a peripheral arterial line; however, it does not provide information on cardiac filling volumes and extravascular lung water. Dilution measurements cannot be performed too frequently, and can be subject to error in the presence of certain muscle relaxants. The PulseCO algorithm used by LiDCO is based on pulse power derivation and is not dependent on waveform morphology.
FloTrac technology
A more recent development is the FloTrac system which can derive cardiac output from the arterial waveform without the need for an independent method of calibration. Hence continuous cardiac output can be measured directly from a conventional arterial line. This method has yet to be extensively evaluated, but early studies suggest that it is accurate. Another similar system that uses the arterial pulse is the pressure recording analytical method (PRAM). Neither the FloTrac nor the PRAM require external calibration.
Impedance plethysmography
This advanced technique was developed by NASA, it measures changing impedance in the chest as the heart beats to calculate cardiac output. This technique has progressed clinically (often called BioZ, i.e. biologic impedance, as promoted by the leading manufacturer in the US) and allows low cost, non-invasive estimations of cardiac output and total peripheral resistance, using only 4 skin electrodes, with minimal removal of clothing in physician offices having the needed equipment.
Equations
By simplifying D'arcy's Law, we get the equation that
When applied to the circulatory system, we get:
Where ABP = Aortic (or Arterial) Blood Pressure, RAP = Right Atrial Pressure and TPR = Total Peripheral Resistance.
However, as ABP>>RAP, and RAP is approximately 0, this can be simplified to:
Physiologists will often re-arrange this equation, making ABP the subject, to study the body's responses.
As has already been stated, Cardiac Output is also the product of the heart rate and the stroke volume, which allows us to say:
From Wikipedia, the free encyclopedia
Cardiac output is the volume of blood being pumped by the heart, in particular a ventricle in a minute. It is equal to the heart rate multiplied by the stroke volume.
Therefore, if there are 70 beats per minute, and 70 ml blood is ejected with each beat of the heart, the cardiac output is 4900 ml/minute. This value is typical for an average adult at rest, although cardiac output may reach up to 30 liters/minute during extreme exercise.
When cardiac output increases in a healthy but untrained individual, most of the increase can be attributed to increase in heart rate. Change of posture, increased sympathetic nervous system activity, and decreased parasympathetic nervous system activity can also increase cardiac output. Heart rate can vary by a factor of approximately 3, between 60 and 180 beats per minute, whilst stroke volume can vary between 70 and 120 ml, a factor of only 1.7.
Contents
1 Measuring Cardiac Output
1.1 The Fick Principle
1.2 Dilution methods
1.3 Doppler method
1.4 Pulmonary Artery Thermodilution (Trans-right-heart Thermodilution)
1.5 PulseCO and PiCCO Technology
1.6 FloTrac technology
1.7 Impedance plethysmography
2 Equations
//
Measuring Cardiac Output
There are many invasive and several non-invasive methods for measuring cardiac output in mammals.
A non-invasive method, often used in teaching students of physiology, reasons as follows:
The pressure in the heart rises as blood is forced into the aorta
The more stretched the aorta, the greater the pulse pressure
In healthy young subjects, each additional 2ml of blood results in a 1 mmHg rise in pressure
Therefore Stroke volume = 2ml x Pulse pressure
Cardiac Output is therefore 2ml x Pulse Pressure x Heart Rate
The Fick Principle
Fick principle involves measuring:
VO2 consumption per minute using a spirometer (with the subject re-breathing air) and a CO2 absorber
the oxygen content of blood taken from the pulmonary artery (representing venous blood)
the oxygen content of blood from a cannula in a peripheral artery (representing arterial blood)
From these values, we know that:
where CO = Cardiac Output, CA = Oxygen concentration of arterial blood and CV = Oxygen concentration of venous blood.
This allows us to say
and therefore calculate cardiac output.
Dilution methods
This method measures how fast flowing blood can dilute an indicator substance introduced to the circulatory system, usually using a pulmonary artery catheter. Early methods used a dye, the cardiac output being inversely proportional to the concentration of dye sampled downstream. More specifically, the cardiac output is equal to the quantity of indicator dye injected divided by the area under the dilution curve measured downstream (the Stewart-Hamilton equation):
The trapezoid rule is often used as an approximation of this integral. A more modern technique is to use cold saline as the indicator, and then measure the change in temperature downstream. Cardiac output can be affected by the phase of respiration, especially under mechanical ventilation, and should therefore be measured at a defined phase of the respiratory cycle (typically end-expiratory).
Doppler method
This technique uses ultrasound and the Doppler effect to measure cardiac output. The blood velocity through the aorta cause a 'Doppler shift' in the frequency of the returning ultrasound waves. Echocardiographic measurement of the aortic root cross-sectional area (or, alternatively, the descending aorta area) multiplied by the measured velocity time integral of flow through that area and heart rate, yields the cardiac output.
Pulmonary Artery Thermodilution (Trans-right-heart Thermodilution)
The pulmonary artery catheter (PAC) also known as the Swan-Ganz thermodilution catheter provides right heart blood pressures. Using the PAC thermodilution cardiac output can be measured. Modern catheters are fitted with a distal heated filament, which allows automatic thermodilution measurement via heating the blood and measuring the resultant thermodilution trace. This provides near continuous cardiac output monitoring. The PAC is used in assessment of haemodynamic status and direct intracardiac and pulmonary artery pressures. The distal (pulmonary artery) port allows sampling of mixed venous blood for the assessment of oxygen transport and the calculation of derived parameters such as oxygen consumption, oxygen utilization coefficient, and intrapulmonary shunt fraction.
The PAC is balloon tipped which can be inflated to occlude the pulmonary artery, the subsequence back pressure is a reflection of the left atrial filling pressure and until recently was considered a good indicator of preload.
The pulmonary artery wedge pressure (PAWP) has been superseded by more reliable techniques such as intrathoracic blood volume or stroke volume variation as indicators of volume status. The PAC also allows sampling of mixed venous blood, the oxygen content of which can be used to indicate the adequacy of overall oxygen delivery. The PAC has fallen out of common use as clinicians favour less invasive, less hazardous technologies for monitoring haemodynamic status. Considerable controversy exists over whether the PAC increases mortality; recent studies suggest it neither increases nor improves mortality. Complications such as cardiac tamponade, pulmonary artery rupture and air emboli are a danger.
PulseCO and PiCCO Technology
PiCCO (PULSION Medical Systems AG, Munich, Germany) and PulseCO (LiDCO Ltd, London, England) generate continuous cardiac output by analysis of the arterial blood pressure waveform. In both cases, an independent technique is required to provide initial calibration of the continuous cardiac output analysis, as arterial waveform analysis cannot account for unmeasured variables such as compliance of the vascular tree.
In the case of PiCCO, transpulmonary thermodilution is used as the independent technique. This uses the Stewart-Hamilton principle outlined above, but measured from central venous line to a central (i.e. femoral or axillary) arterial line. The cardiac output derived from this cold-saline thermodilution is used to calibrate the arterial pulse contour analysis, which can then provide continuous cardiac output monitoring. The PiCCO algorithm is dependent on blood pressure waveform morphology (i.e. mathematical analysis of the pulse contour waveform) and calculates continuous cardiac output as described by Wesseling and co-workers. Transpulmonary thermodilution spans right heart, pulmonary circulation and left heart; this allows further mathematical analysis of the thermodilution curve, giving measurements of cardiac filling volumes (GEDV), intrathoracic blood volume, and extravascular lung water.
In the case of LiDCO, the independent calibration technique is lithium dilution, again using the Stewart-Hamilton principle. Lithium dilution has the advantage of being usable from a peripheral vein to a peripheral arterial line; however, it does not provide information on cardiac filling volumes and extravascular lung water. Dilution measurements cannot be performed too frequently, and can be subject to error in the presence of certain muscle relaxants. The PulseCO algorithm used by LiDCO is based on pulse power derivation and is not dependent on waveform morphology.
FloTrac technology
A more recent development is the FloTrac system which can derive cardiac output from the arterial waveform without the need for an independent method of calibration. Hence continuous cardiac output can be measured directly from a conventional arterial line. This method has yet to be extensively evaluated, but early studies suggest that it is accurate. Another similar system that uses the arterial pulse is the pressure recording analytical method (PRAM). Neither the FloTrac nor the PRAM require external calibration.
Impedance plethysmography
This advanced technique was developed by NASA, it measures changing impedance in the chest as the heart beats to calculate cardiac output. This technique has progressed clinically (often called BioZ, i.e. biologic impedance, as promoted by the leading manufacturer in the US) and allows low cost, non-invasive estimations of cardiac output and total peripheral resistance, using only 4 skin electrodes, with minimal removal of clothing in physician offices having the needed equipment.
Equations
By simplifying D'arcy's Law, we get the equation that
When applied to the circulatory system, we get:
Where ABP = Aortic (or Arterial) Blood Pressure, RAP = Right Atrial Pressure and TPR = Total Peripheral Resistance.
However, as ABP>>RAP, and RAP is approximately 0, this can be simplified to:
Physiologists will often re-arrange this equation, making ABP the subject, to study the body's responses.
As has already been stated, Cardiac Output is also the product of the heart rate and the stroke volume, which allows us to say:
Afterload
Ventricular systole. (Red arrow is path from left ventricle to aorta. Afterload is largely dependent upon aortic pressure.In cardiac physiology, afterload is the tension produced by a chamber of the heart in order to contract. If the chamber is not mentioned, it is usually assumed to be the left ventricle.
Afterload can also be described as the pressure that the chamber of the heart has to generate in order to eject blood out of the chamber. Everything else held equal, as afterload increases, cardiac output decreases.
In the case of the left ventricle, the afterload is a consequence of the blood pressure, since the pressure in the ventricle must be greater than the blood pressure in order to open the aortic valve.
Pathology
Disease processes that increase the left ventricular afterload include increased blood pressure and aortic valve disease.
Hypertension (Increased blood pressure) increases the left ventricular afterload because the left ventricle has to work harder to eject blood into the aorta. This is because the aortic valve won't open until the pressure generated in the left ventricle is higher than the elevated blood pressure.
Aortic stenosis increases the afterload because the left ventricle has to overcome the pressure gradient caused by the stenotic aortic valve in addition to the blood pressure in order to eject blood into the aorta. For instance, if the blood pressure is 120/80, and the aortic valve stenosis creates a trans-valvular gradient of 30 mmHg, the left ventricle has to generate a pressure of 150 mmHg in order to open the aortic valve and eject blood into the aorta.
Aortic insufficiency increases afterload because a percentage of the blood that is ejected forward regurgitates back through the diseased aortic valve. This leads to elevated systolic blood pressure.
Mitral regurgitation decreases the afterload. During ventricular systole, the blood can regurgitate through the diseased mitral valve as well as be ejected through the aortic valve. This means that the left ventricle has to work less to eject blood, causing a decreased afterload.
See also
Preload Cardiac output
Afterload
Preload (cardiology)
Heart during ventricular diastole.
In cardiac physiology, preload is the volume of blood present in a ventricle of the heart, after passive filling and atrial contraction. If the chamber is not mentioned, it is usually assumed to be the left ventricle.
Preload is theoretically most accurately described as the initial stretching of cardiac myocytes prior to contraction. This cannot be measured in vivo and therefore other measurements are used as estimates. Estimation is inaccurate, for example in a chronically dilated ventricle new sarcomeres may have formed in the heart muscle allowing the relaxed ventricle to appear enlarged.
Preload is affected by venous blood pressure and the rate of venous return. These are affected by venous tone and volume of circulating blood.
Preload is the ventricular End-diastolic volume. Preload increases with exercise (slightly), increasing blood volume (overtransfusion) and excitement (sympathetics).
See also
Afterload
Cardiac output Frank-Starling law of the heart
In cardiac physiology, preload is the volume of blood present in a ventricle of the heart, after passive filling and atrial contraction. If the chamber is not mentioned, it is usually assumed to be the left ventricle.
Preload is theoretically most accurately described as the initial stretching of cardiac myocytes prior to contraction. This cannot be measured in vivo and therefore other measurements are used as estimates. Estimation is inaccurate, for example in a chronically dilated ventricle new sarcomeres may have formed in the heart muscle allowing the relaxed ventricle to appear enlarged.
Preload is affected by venous blood pressure and the rate of venous return. These are affected by venous tone and volume of circulating blood.
Preload is the ventricular End-diastolic volume. Preload increases with exercise (slightly), increasing blood volume (overtransfusion) and excitement (sympathetics).
See also
Afterload
Cardiac output Frank-Starling law of the heart
Aortic valve replacement
Aortic valve replacement is a surgical procedure in which a patient's aortic valve is replaced by a different valve. The aortic valve can be affected by a range of diseases and require aortic valve replacement. The valve can either become leaky (regurgitant or insufficient) or stuck partially shut (stenotic). Aortic valve replacement currently requires open heart surgery. As of 2006, percutaneous aortic valve replacement is being researched, which allows the implantion of valves using a catheter without open heart surgery.
Contents
• 1 Types of Heart Valves
o 1.1 Mechanical, Tissue and Homograft Valves
o 1.2 Durability
• 2 Surgical Procedure
• 3 Hospital Stay and Recovery Time
• 4 Surgical Outcome and Risk of Procedure
• 5 See also
Types of Heart Valves
Mechanical, Tissue and Homograft Valves
There are two basic types of artificial heart valve, mechanical valves and tissue valves. Tissue heart valves are usually made from animal tissues, either animal heart valve tissue or animal pericardial tissue. The tissue is treated to prevent rejection and to prevent calcification.
There are alternatives to animal tissue valves. In some cases a human aortic valve can be implanted. These are called homografts. Homograft valves are donated by patients and harvested after the patient expires. The durability of homograft valves is probably the same for porcine tissue valves. Another procedure for aortic valve replacement is the Ross procedure or pulmonary autograft. The Ross procedure, named after Dr. Donald Ross - one of the pioneers in cardiac surgery in the U.K., is surgery where the aortic valve is removed and replaced with the patient's own pulmonary valve. A pulmonary homograft (pulmonary valve taken from a cadaver) is then used to replace the patients own pulmonary valve. This procedure was first used in 1967.
Although mechanical valves are long-lasting and generally only one surgery is needed, there is an increased risk of blood clots forming with mechanical valves. As a result, mechanical valve recipients must generally take anti-coagulant drugs such as warfarin for the rest of their lives, which effectively makes them borderline hemophiliacs.
Durability
Mechanical valves are designed to outlast the patient, and have typically been stress-tested to last several hundred years. Tissue valves will typically last between 10-15 years. In younger patients, tissue valves will wear out faster. For this reason, older patients are often recommended tissue valves.
Surgical Procedure
Aortic valve replacement is most frequently done through a median sternotomy, meaning the chestbone is sawed through. Once the pericardium has been opened, the patient is placed on cardiopulmonary bypass machine, also referred to as the heart-lung machine. This machine takes over the task of breathing for the patient and pumping his blood around while the surgeon replaces the heart valve.
Once the patient is on bypass, an incision is made in the aorta. The surgeon then removes the patient's diseased aortic valve and a mechanical or tissue valve is put in its place. Once the valve is in place and the aorta has been closed, the patient is taken off the heart-lung machine. Transesophageal echocardiogram (or TEE, an ultra-sound of the heart done through the esophagus) can be used to verify that the new valve is functioning properly. Pacing wires are usually put in place, so that the heart can be manually paced should any complications arise after surgery. Drainage tubes are also inserted to drain fluids from the chest and pericardium following surgery. These are usually removed within 36 hours while the pacing wires are generally left in place until right before the patient is discharged from the hospital.
Hospital Stay and Recovery Time
Immediately after aortic valve replacement, the patient will frequently stay in a Cardiothoracic Intensive Care Unit for 12-36 hours. After this, the patient is often moved to a lower-dependency unit and then to a cardiac surgery ward. Total time spent in hospital following surgery is usually between 4 and 10 days, unless complications arise.
Recovery from aortic valve replacement will take 1-3 months if the patient is in good health. Patients are advised not to do any heavy lifting for 6-8 weeks following surgery to avoid damaging the sternum (breast bone) while it heals.
Surgical Outcome and Risk of Procedure
The risk of death or serious complications from aortic valve replacement is typically quoted as being between 1-5%, depending on the health and age of the patient, as well as the skill of the surgeon. Older patients, as well as more fragile ones, are sometimes inelegible for surgery because of elevated risks.
See also
• Aortic valve repair
• Mitral valve repair
Mitral valve repair
From Wikipedia, the free encyclopedia
Mitral valve repair is an open heart procedure performed by cardiothoracic surgeons to treat stenosis (narrowing) or regurgitation (leakage) of the mitral valve. The mitral valve is the "inflow valve" for the left side of the heart. Blood flows from the lungs, where it picks up oxygen, and into the heart through the mitral valve. When it opens, the mitral valve allows blood to flow into the heart's main pumping chamber called the left ventricle. It then closes to keep blood from leaking back into the lungs when the ventricle contracts (squeezes) to push blood out to the body. It has two flaps, or leaflets.
The techniques of mitral valve repair include inserting a cloth-covered ring around the valve to bring the leaflets into contact with each other (annuloplasty), removal of redundant/loose segments of the leaflets (quadrangular resection), re-suspension of the leaflets with artificial (Gore-Tex) cords, and more recently the "bow-tie" procedure where a single stitch allows to repair the valve non-surgically.
Occasionally, the mitral valve is abnormal from birth (congenital). More often the mitral valve becomes abnormal with age (degenerative) or as a result of rheumatic fever. In rare instances the mitral valve can be destroyed by infection or a bacterial endocarditis. Mitral regurgitation may also occur as a result of ischemic heart disease (coronary artery disease).
A history of mitral valve repair
The development of the heart-lung machine in the 1950s paved the way for replacement of the mitral valve with an artificial valve in the 1960s. For decades, mitral valve replacement was the standard operation for a patient with a diseased mitral valve.
There are significant downsides to an artificial mitral valve. Infection of the prosthetic valve can occur, which is very dangerous. Patients with mechanical heart valves are required to take blood thinners for the rest of their lives and are at risk for bleeding complications. Artificial tissue valves will last between 10 and 15 years, placing the patient at risk of a second operation to replace the valve. The risk of stroke with an artificial mitral valve is significant (approximately 1 % per year).
In the last two decades, some surgeons have embraced surgical techniques to repair, rather than replace, the mitral valve. These techniques were pioneered by a French heart surgeon, Dr. Alain F. Carpentier, who published a landmark paper in the mid 1980s entitled The French Correction.
See also
• Aortic valve repair
• Cardiac surgery
Contents
• 1 Types of Heart Valves
o 1.1 Mechanical, Tissue and Homograft Valves
o 1.2 Durability
• 2 Surgical Procedure
• 3 Hospital Stay and Recovery Time
• 4 Surgical Outcome and Risk of Procedure
• 5 See also
Types of Heart Valves
Mechanical, Tissue and Homograft Valves
There are two basic types of artificial heart valve, mechanical valves and tissue valves. Tissue heart valves are usually made from animal tissues, either animal heart valve tissue or animal pericardial tissue. The tissue is treated to prevent rejection and to prevent calcification.
There are alternatives to animal tissue valves. In some cases a human aortic valve can be implanted. These are called homografts. Homograft valves are donated by patients and harvested after the patient expires. The durability of homograft valves is probably the same for porcine tissue valves. Another procedure for aortic valve replacement is the Ross procedure or pulmonary autograft. The Ross procedure, named after Dr. Donald Ross - one of the pioneers in cardiac surgery in the U.K., is surgery where the aortic valve is removed and replaced with the patient's own pulmonary valve. A pulmonary homograft (pulmonary valve taken from a cadaver) is then used to replace the patients own pulmonary valve. This procedure was first used in 1967.
Although mechanical valves are long-lasting and generally only one surgery is needed, there is an increased risk of blood clots forming with mechanical valves. As a result, mechanical valve recipients must generally take anti-coagulant drugs such as warfarin for the rest of their lives, which effectively makes them borderline hemophiliacs.
Durability
Mechanical valves are designed to outlast the patient, and have typically been stress-tested to last several hundred years. Tissue valves will typically last between 10-15 years. In younger patients, tissue valves will wear out faster. For this reason, older patients are often recommended tissue valves.
Surgical Procedure
Aortic valve replacement is most frequently done through a median sternotomy, meaning the chestbone is sawed through. Once the pericardium has been opened, the patient is placed on cardiopulmonary bypass machine, also referred to as the heart-lung machine. This machine takes over the task of breathing for the patient and pumping his blood around while the surgeon replaces the heart valve.
Once the patient is on bypass, an incision is made in the aorta. The surgeon then removes the patient's diseased aortic valve and a mechanical or tissue valve is put in its place. Once the valve is in place and the aorta has been closed, the patient is taken off the heart-lung machine. Transesophageal echocardiogram (or TEE, an ultra-sound of the heart done through the esophagus) can be used to verify that the new valve is functioning properly. Pacing wires are usually put in place, so that the heart can be manually paced should any complications arise after surgery. Drainage tubes are also inserted to drain fluids from the chest and pericardium following surgery. These are usually removed within 36 hours while the pacing wires are generally left in place until right before the patient is discharged from the hospital.
Hospital Stay and Recovery Time
Immediately after aortic valve replacement, the patient will frequently stay in a Cardiothoracic Intensive Care Unit for 12-36 hours. After this, the patient is often moved to a lower-dependency unit and then to a cardiac surgery ward. Total time spent in hospital following surgery is usually between 4 and 10 days, unless complications arise.
Recovery from aortic valve replacement will take 1-3 months if the patient is in good health. Patients are advised not to do any heavy lifting for 6-8 weeks following surgery to avoid damaging the sternum (breast bone) while it heals.
Surgical Outcome and Risk of Procedure
The risk of death or serious complications from aortic valve replacement is typically quoted as being between 1-5%, depending on the health and age of the patient, as well as the skill of the surgeon. Older patients, as well as more fragile ones, are sometimes inelegible for surgery because of elevated risks.
See also
• Aortic valve repair
• Mitral valve repair
Mitral valve repair
From Wikipedia, the free encyclopedia
Mitral valve repair is an open heart procedure performed by cardiothoracic surgeons to treat stenosis (narrowing) or regurgitation (leakage) of the mitral valve. The mitral valve is the "inflow valve" for the left side of the heart. Blood flows from the lungs, where it picks up oxygen, and into the heart through the mitral valve. When it opens, the mitral valve allows blood to flow into the heart's main pumping chamber called the left ventricle. It then closes to keep blood from leaking back into the lungs when the ventricle contracts (squeezes) to push blood out to the body. It has two flaps, or leaflets.
The techniques of mitral valve repair include inserting a cloth-covered ring around the valve to bring the leaflets into contact with each other (annuloplasty), removal of redundant/loose segments of the leaflets (quadrangular resection), re-suspension of the leaflets with artificial (Gore-Tex) cords, and more recently the "bow-tie" procedure where a single stitch allows to repair the valve non-surgically.
Occasionally, the mitral valve is abnormal from birth (congenital). More often the mitral valve becomes abnormal with age (degenerative) or as a result of rheumatic fever. In rare instances the mitral valve can be destroyed by infection or a bacterial endocarditis. Mitral regurgitation may also occur as a result of ischemic heart disease (coronary artery disease).
A history of mitral valve repair
The development of the heart-lung machine in the 1950s paved the way for replacement of the mitral valve with an artificial valve in the 1960s. For decades, mitral valve replacement was the standard operation for a patient with a diseased mitral valve.
There are significant downsides to an artificial mitral valve. Infection of the prosthetic valve can occur, which is very dangerous. Patients with mechanical heart valves are required to take blood thinners for the rest of their lives and are at risk for bleeding complications. Artificial tissue valves will last between 10 and 15 years, placing the patient at risk of a second operation to replace the valve. The risk of stroke with an artificial mitral valve is significant (approximately 1 % per year).
In the last two decades, some surgeons have embraced surgical techniques to repair, rather than replace, the mitral valve. These techniques were pioneered by a French heart surgeon, Dr. Alain F. Carpentier, who published a landmark paper in the mid 1980s entitled The French Correction.
See also
• Aortic valve repair
• Cardiac surgery
Aortic insufficiency
Aortic insufficiency
Aortic insufficiency (AI), also known as aortic regurgitation (AR), is the leaking of the aortic valve of the heart that causes blood to flow in the reverse direction during ventricular diastole, from the aorta into the left ventricle.
Aortic insufficiency can be due to abnormalities of either the aortic valve or the aortic root (the beginning of the aorta).
Contents
1 Etiology
2 Physiology
3 Pathophysiology
4 Hemodynamics
4.1 Acute aortic insufficiency
4.2 Chronic aortic insufficiency
5 Physical examination
6 Diagnostic evaluation
7 Prognosis
8 Treatment
8.1 Medical treatment
8.2 Surgical treatment
9 References
10 See also
//
Etiology
About half of the cases of aortic insufficiency are due to the aortic root dilatation (annuloaortic ectasia), which is idiopathic in over 80% of cases, but otherwise occurs with aging and hypertension, Marfan syndrome, aortic dissection, and syphilis. In about 15% the cause is innate bicuspidal aortic valve, while another 15% cases are due to retraction of the cusps as part of postinflammatory processes of endocarditis in rheumatic fever and various collagen vascular diseases.
Physiology
In individuals with a normally functioning aortic valve, the valve is only open when the pressure in the left ventricle is higher than the pressure in the aorta. This allows the blood to be ejected from the left ventricle into the aorta during ventricular systole. After ventricular systole, the pressure in the ventricle decreases, as the ventricle relaxes and gets ready to fill up with blood from the left atrium. This relaxation of the left ventricle (early ventricular diastole) causes a fall in the pressure in the left ventricle. When the pressure in the left ventricle falls below the pressure in the aorta, the aortic valve will close, preventing blood from going from the aorta back into the left ventricle. The amount of blood that is ejected by the heart is known as the stroke volume or stroke work. Under normal conditions, the entire stroke volume delivers oxygenated blood to the body.
Pathophysiology
In aortic insufficiency, when the pressure in the left ventricle falls below the pressure in the aorta, the aortic valve is not able to completely close. This causes a leaking of blood from the aorta into the left ventricle. This means that some of the blood that was already ejected from the heart is regurgitating back into the heart. The percentage of blood that regurgitates back through the aortic valve due to AI is known as the regurgitant fraction. For instance, if an individual with AI has a stroke volume of 100 ml and during ventricular diastole 25 ml regurgitates back through the aortic valve, the regurgitant fraction is 25%. This regurgitant flow causes a decrease in the diastolic blood pressure in the aorta, and therefore an increase in the pulse pressure (systolic pressure - diastolic pressure)- not to be confounded with hypertension.
Since some of the blood that is ejected during systole regurgitates back during diastole, there is decreased effective forward flow in AI.
AI causes both volume overload (elevated preload) and pressure overload (elevated afterload) of the heart.
The pressure overload (due to elevated pulse pressure and hypertension) causes left ventricular hypertrophy (LVH). There is both concentric hypertrophy and eccentric hypertrophy in AI. The concentric hypertrophy is due to the hypertension associated with AI, while the eccentric hypertrophy is due to volume overload caused by the regurgitant fraction.
Hemodynamics
The hemodynamic sequelae of AI are dependent on the rate of onset of AI. Acute AI and chronic AI will have different hemodynamics and individuals will have different signs and symptoms.
[edit] Acute aortic insufficiency
In acute AI, as may be seen with acute perforation of the aortic valve due to endocarditis, there will be a sudden increase in the volume of blood in the left ventricle. The ventricle, unable to deal with the sudden change in volume, decompensates. The filling pressure of the left ventricle will increase. This causes pressure in the left atrium to rise, and the individual will develop congestive heart failure.
Severe acute aortic insufficiency is considered a medical emergency. There is a high mortality rate if the individual does not undergo immediate surgery for aortic valve replacement. If the acute AI is due to aortic valve endocarditis, there is a risk that the new valve may become seeded with bacteria. However, this risk is small.1
Acute AI may be difficult to diagnose clinically, since the left ventricle had not yet developed the eccentric hypertrophy and dilatation that allow an increased stroke volume and bounding peripheral pulses that are common in chronic AI. On auscultation, there may be a short diastolic murmur and a soft S1. S1 is soft because the elevated filling pressures close the mitral valve in diastole (rather than the mitral valve being closed at the beginning of systole).
Chronic aortic insufficiency
If the individual survives the initial hemodynamic derailment that acute AI presents as, the left ventricle adapts by eccentric hypertrophy and dilatation of the left ventricle, and the volume overload is compensated for. The left ventricular filling pressures will revert to normal and the individual will no longer have overt heart failure.
In this compensated phase, the individual may be totally asymptomatic and may have normal exercise tolerance.
Eventually (typically after a latency period) the left ventricle will become decompensated, and filling pressures will increase. While most individuals would complain of symptoms of congestive heart failure to their physicians, some enter this decompensated phase asymptomatically. Proper treatment for AI involves aortic valve replacement prior to this decompensation phase.
Physical examination
The physical examination of an individual with aortic insufficiency involves auscultation of the heart to listen for the murmur of aortic insufficiency and related heart sounds. The murmur of chronic aortic insufficiency is typically desribed as early diastolic and decresendo, which is best heard at aortic area when the patient is sitted and leans forward with breath held in expiration. The murmur is usually soft and seldom causes thrill. If there is radiation to the right parasternal region, ascending aortic aneurysm has to be excluded.
There is there increased stroke volume of the left ventricle due to volume overload, an ejection systolic 'flow' murmur may also be present when auscultating the same aortic area. Unless there is cocomittant aortic valve stenosis, the murmur should not start with an ejection click.
There may also be an Austin Flint murmur, a soft mid-diastolic rumble heard at the apical area. It appears when regurgitant jet from the severe aortic insufficiency renders partial closure of the anterior mitral leaflet.
Peripheral physical signs of aortic insufficiency are related to the high pulse pressure and the rapid decrease in blood pressure during diastole due to the AI:
large-volume, 'collapsing' pulse
bounding peripheral pulses; also known as Watson's water hammer pulse
low diastolic and increased pulse pressure
Corrigan's pulse (rapid upstroke and collapse of the carotid artery pulse)
de Musset's sign (head nodding in time with the heart beat)
Quincke's sign (pulsation of the capillary bed in the nail)
Duroziez's sign (systolic and diastolic murmurs described as 'pistol shots' heard over the femoral artery when it is gradually compressed)
Traube's sign (a double sound heard over the femoral artery when it is compressed distally)
Rarer signs include:
Lighthouse sign (blanching & flushing of forehead)
Ladolfi's sign (alternating constriction & dilatation of pupil)
Becker's sign (pulsations of retinal vessels)
Müller's sign (pulsations of uvula)
Mayen's sign (diastolic drop of BP>15 mm Hg with arm raised)
Rosenbach's sign (pulsatile liver)
Gerhardt's sign (enlarged spleen)
Hill's sign (A ≥ 20 mmHg difference in popliteal and brachial systolic cuff pressures, seen in chronic severe AI)
[[Lincoln sign (pulsatile popliteal)
Sherman sign (dorsalis pedis pulse is quickly located & unexpectedly prominent in age>75 yr)
Diagnostic evaluation
The most common test used for the evaluation of the severity of aortic insufficiency is the echocardiogram, which can provide two-dimensional views of the regurgitant jet, and allow measurement of the velocity and volume of the jet.
The echocardiographic findings in severe aortic regurgitation include:
An AI color jet dimension > 60 percent of the left ventricular outflow tract (LVOT) diameter (may not be true if the jet is eccentric)
The pressure half-time of the regurgitant jet is < title="Millisecond" href="http://en.wikipedia.org/wiki/Millisecond">mserly termination of the mitral inflow (due to increase in LV pressure due to the AI.)
Early diastolic flow reversal in the descending aorta.
Regurgitant volume > 60 ml
Regurgitant fraction > 55 percent
Prognosis
The risk of death in individuals with aortic insufficiency, dilated ventricle, normal ejection fraction who are asymptomatic is about 0.2 percent per year. Risk increases if the ejection fraction decreases or if the individual develops symptoms.
Treatment
Indications for surgery for chronic severe aortic insufficiency2
Symptoms
Ejection fraction
Other information
NYHA class III - IV
≥ 50 %
NYHA class II
≥ 50 %
Progression of symptoms or worsoning parameters on echocardiography
CHA class ≥ II angina
≥ 50 %
Regardless of symptoms
25 - 49 %
Cardiac surgery for other cause (ie: CAD, other valvular disease, ascending aortic aneurysm)
Aortic insufficiency can be treated either medically or surgically, depending on the acuteness of presentation, the symptoms and signs associated with the disease process, and the degree of left ventricular dysfunction.
Surgical treatment is typically warranted prior to the ejection fraction falling below 55% or the left ventricular end-systolic dimension falling below 55mm, regardless of symptoms. If either of these thresholds is passed, the prognosis worsens.
Medical treatment
Medical therapy of chronic aortic insufficiency involves the use of vasodilators. Small trials have shown a short term benefit in the use of ACE inhibitors, nifedipine, and hydralazine in improving left ventricular wall stress, ejection fraction, and mass. The use of these vasodilators is only indicated in individuals who suffer from hypertension in addition to AI. The goal in using the use of these pharmacologic agents is to decrease the afterload so that the left ventricle is spared somewhat. The regurgitant fraction may not change significantly, since the gradient between the aortic and left ventricular pressures is usually fairly low at the initiation of treatment.
Surgical treatment
The surgical treatment of choice at this time is an aortic valve replacement. This is currently an open-heart procedure, requiring the individual to be placed on cardiopulmonary bypass.
In the case of severe acute aortic insufficiency, all individuals should undergo surgery if there are no absolute contraindications for surgery. Individuals with bacteremia with aortic valve endocarditis should not wait for treatment with antibiotics to take effect, given the high mortality associated with the acute AI. In stead, replacement with an aortic valve homograft should be performed if feasible.
In the future, it is believed that a percutaneous approach to aortic valve replacement will be feasible.
References
1. al Jubair K, al Fagih MR, Ashmeg A, Belhaj M, Sawyer W. Cardiac operations during active endocarditis. J Thorac Cardiovasc Surg. 1992 Aug;104(2):487-90. (Medline abstract)
2. Bonow et al., ACC/AHA Task Force Report. ACC/AHA Guidelines for the Management of Patients With Valvular Heart Disease. JACC Vol. 32, No. 5, November 1998:1486-1588 (Full article)
See also
Aortic valve replacement
Preload
Afterload
Aortic insufficiency (AI), also known as aortic regurgitation (AR), is the leaking of the aortic valve of the heart that causes blood to flow in the reverse direction during ventricular diastole, from the aorta into the left ventricle.
Aortic insufficiency can be due to abnormalities of either the aortic valve or the aortic root (the beginning of the aorta).
Contents
1 Etiology
2 Physiology
3 Pathophysiology
4 Hemodynamics
4.1 Acute aortic insufficiency
4.2 Chronic aortic insufficiency
5 Physical examination
6 Diagnostic evaluation
7 Prognosis
8 Treatment
8.1 Medical treatment
8.2 Surgical treatment
9 References
10 See also
//
Etiology
About half of the cases of aortic insufficiency are due to the aortic root dilatation (annuloaortic ectasia), which is idiopathic in over 80% of cases, but otherwise occurs with aging and hypertension, Marfan syndrome, aortic dissection, and syphilis. In about 15% the cause is innate bicuspidal aortic valve, while another 15% cases are due to retraction of the cusps as part of postinflammatory processes of endocarditis in rheumatic fever and various collagen vascular diseases.
Physiology
In individuals with a normally functioning aortic valve, the valve is only open when the pressure in the left ventricle is higher than the pressure in the aorta. This allows the blood to be ejected from the left ventricle into the aorta during ventricular systole. After ventricular systole, the pressure in the ventricle decreases, as the ventricle relaxes and gets ready to fill up with blood from the left atrium. This relaxation of the left ventricle (early ventricular diastole) causes a fall in the pressure in the left ventricle. When the pressure in the left ventricle falls below the pressure in the aorta, the aortic valve will close, preventing blood from going from the aorta back into the left ventricle. The amount of blood that is ejected by the heart is known as the stroke volume or stroke work. Under normal conditions, the entire stroke volume delivers oxygenated blood to the body.
Pathophysiology
In aortic insufficiency, when the pressure in the left ventricle falls below the pressure in the aorta, the aortic valve is not able to completely close. This causes a leaking of blood from the aorta into the left ventricle. This means that some of the blood that was already ejected from the heart is regurgitating back into the heart. The percentage of blood that regurgitates back through the aortic valve due to AI is known as the regurgitant fraction. For instance, if an individual with AI has a stroke volume of 100 ml and during ventricular diastole 25 ml regurgitates back through the aortic valve, the regurgitant fraction is 25%. This regurgitant flow causes a decrease in the diastolic blood pressure in the aorta, and therefore an increase in the pulse pressure (systolic pressure - diastolic pressure)- not to be confounded with hypertension.
Since some of the blood that is ejected during systole regurgitates back during diastole, there is decreased effective forward flow in AI.
AI causes both volume overload (elevated preload) and pressure overload (elevated afterload) of the heart.
The pressure overload (due to elevated pulse pressure and hypertension) causes left ventricular hypertrophy (LVH). There is both concentric hypertrophy and eccentric hypertrophy in AI. The concentric hypertrophy is due to the hypertension associated with AI, while the eccentric hypertrophy is due to volume overload caused by the regurgitant fraction.
Hemodynamics
The hemodynamic sequelae of AI are dependent on the rate of onset of AI. Acute AI and chronic AI will have different hemodynamics and individuals will have different signs and symptoms.
[edit] Acute aortic insufficiency
In acute AI, as may be seen with acute perforation of the aortic valve due to endocarditis, there will be a sudden increase in the volume of blood in the left ventricle. The ventricle, unable to deal with the sudden change in volume, decompensates. The filling pressure of the left ventricle will increase. This causes pressure in the left atrium to rise, and the individual will develop congestive heart failure.
Severe acute aortic insufficiency is considered a medical emergency. There is a high mortality rate if the individual does not undergo immediate surgery for aortic valve replacement. If the acute AI is due to aortic valve endocarditis, there is a risk that the new valve may become seeded with bacteria. However, this risk is small.1
Acute AI may be difficult to diagnose clinically, since the left ventricle had not yet developed the eccentric hypertrophy and dilatation that allow an increased stroke volume and bounding peripheral pulses that are common in chronic AI. On auscultation, there may be a short diastolic murmur and a soft S1. S1 is soft because the elevated filling pressures close the mitral valve in diastole (rather than the mitral valve being closed at the beginning of systole).
Chronic aortic insufficiency
If the individual survives the initial hemodynamic derailment that acute AI presents as, the left ventricle adapts by eccentric hypertrophy and dilatation of the left ventricle, and the volume overload is compensated for. The left ventricular filling pressures will revert to normal and the individual will no longer have overt heart failure.
In this compensated phase, the individual may be totally asymptomatic and may have normal exercise tolerance.
Eventually (typically after a latency period) the left ventricle will become decompensated, and filling pressures will increase. While most individuals would complain of symptoms of congestive heart failure to their physicians, some enter this decompensated phase asymptomatically. Proper treatment for AI involves aortic valve replacement prior to this decompensation phase.
Physical examination
The physical examination of an individual with aortic insufficiency involves auscultation of the heart to listen for the murmur of aortic insufficiency and related heart sounds. The murmur of chronic aortic insufficiency is typically desribed as early diastolic and decresendo, which is best heard at aortic area when the patient is sitted and leans forward with breath held in expiration. The murmur is usually soft and seldom causes thrill. If there is radiation to the right parasternal region, ascending aortic aneurysm has to be excluded.
There is there increased stroke volume of the left ventricle due to volume overload, an ejection systolic 'flow' murmur may also be present when auscultating the same aortic area. Unless there is cocomittant aortic valve stenosis, the murmur should not start with an ejection click.
There may also be an Austin Flint murmur, a soft mid-diastolic rumble heard at the apical area. It appears when regurgitant jet from the severe aortic insufficiency renders partial closure of the anterior mitral leaflet.
Peripheral physical signs of aortic insufficiency are related to the high pulse pressure and the rapid decrease in blood pressure during diastole due to the AI:
large-volume, 'collapsing' pulse
bounding peripheral pulses; also known as Watson's water hammer pulse
low diastolic and increased pulse pressure
Corrigan's pulse (rapid upstroke and collapse of the carotid artery pulse)
de Musset's sign (head nodding in time with the heart beat)
Quincke's sign (pulsation of the capillary bed in the nail)
Duroziez's sign (systolic and diastolic murmurs described as 'pistol shots' heard over the femoral artery when it is gradually compressed)
Traube's sign (a double sound heard over the femoral artery when it is compressed distally)
Rarer signs include:
Lighthouse sign (blanching & flushing of forehead)
Ladolfi's sign (alternating constriction & dilatation of pupil)
Becker's sign (pulsations of retinal vessels)
Müller's sign (pulsations of uvula)
Mayen's sign (diastolic drop of BP>15 mm Hg with arm raised)
Rosenbach's sign (pulsatile liver)
Gerhardt's sign (enlarged spleen)
Hill's sign (A ≥ 20 mmHg difference in popliteal and brachial systolic cuff pressures, seen in chronic severe AI)
[[Lincoln sign (pulsatile popliteal)
Sherman sign (dorsalis pedis pulse is quickly located & unexpectedly prominent in age>75 yr)
Diagnostic evaluation
The most common test used for the evaluation of the severity of aortic insufficiency is the echocardiogram, which can provide two-dimensional views of the regurgitant jet, and allow measurement of the velocity and volume of the jet.
The echocardiographic findings in severe aortic regurgitation include:
An AI color jet dimension > 60 percent of the left ventricular outflow tract (LVOT) diameter (may not be true if the jet is eccentric)
The pressure half-time of the regurgitant jet is < title="Millisecond" href="http://en.wikipedia.org/wiki/Millisecond">mserly termination of the mitral inflow (due to increase in LV pressure due to the AI.)
Early diastolic flow reversal in the descending aorta.
Regurgitant volume > 60 ml
Regurgitant fraction > 55 percent
Prognosis
The risk of death in individuals with aortic insufficiency, dilated ventricle, normal ejection fraction who are asymptomatic is about 0.2 percent per year. Risk increases if the ejection fraction decreases or if the individual develops symptoms.
Treatment
Indications for surgery for chronic severe aortic insufficiency2
Symptoms
Ejection fraction
Other information
NYHA class III - IV
≥ 50 %
NYHA class II
≥ 50 %
Progression of symptoms or worsoning parameters on echocardiography
CHA class ≥ II angina
≥ 50 %
Regardless of symptoms
25 - 49 %
Cardiac surgery for other cause (ie: CAD, other valvular disease, ascending aortic aneurysm)
Aortic insufficiency can be treated either medically or surgically, depending on the acuteness of presentation, the symptoms and signs associated with the disease process, and the degree of left ventricular dysfunction.
Surgical treatment is typically warranted prior to the ejection fraction falling below 55% or the left ventricular end-systolic dimension falling below 55mm, regardless of symptoms. If either of these thresholds is passed, the prognosis worsens.
Medical treatment
Medical therapy of chronic aortic insufficiency involves the use of vasodilators. Small trials have shown a short term benefit in the use of ACE inhibitors, nifedipine, and hydralazine in improving left ventricular wall stress, ejection fraction, and mass. The use of these vasodilators is only indicated in individuals who suffer from hypertension in addition to AI. The goal in using the use of these pharmacologic agents is to decrease the afterload so that the left ventricle is spared somewhat. The regurgitant fraction may not change significantly, since the gradient between the aortic and left ventricular pressures is usually fairly low at the initiation of treatment.
Surgical treatment
The surgical treatment of choice at this time is an aortic valve replacement. This is currently an open-heart procedure, requiring the individual to be placed on cardiopulmonary bypass.
In the case of severe acute aortic insufficiency, all individuals should undergo surgery if there are no absolute contraindications for surgery. Individuals with bacteremia with aortic valve endocarditis should not wait for treatment with antibiotics to take effect, given the high mortality associated with the acute AI. In stead, replacement with an aortic valve homograft should be performed if feasible.
In the future, it is believed that a percutaneous approach to aortic valve replacement will be feasible.
References
1. al Jubair K, al Fagih MR, Ashmeg A, Belhaj M, Sawyer W. Cardiac operations during active endocarditis. J Thorac Cardiovasc Surg. 1992 Aug;104(2):487-90. (Medline abstract)
2. Bonow et al., ACC/AHA Task Force Report. ACC/AHA Guidelines for the Management of Patients With Valvular Heart Disease. JACC Vol. 32, No. 5, November 1998:1486-1588 (Full article)
See also
Aortic valve replacement
Preload
Afterload
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