Cardiac output is a measure of the volume of blood pumped by the heart within a particular timeframe (normally measured in L/min). It is calculated by CO = Stroke volume x Heart rate, where the stroke volume gives the volume pumped per beat, and heart rate gives the beats per minute. Cardiac output is not a constant figure and changes depending on a number of variables, most notably venous return (volume of blood returning to the heart) which determines the end-diastolic volume of the heart (volume of blood after contraction of the atria results in the filling of the ventricles).
Changing Heart Rate will change the cardiac output. Heart rate commonly increases in response to exertion or emotional stress. The change is effected by either an increase in sympathetic stimulation of the heart, or a decrease in stimulation by the parasympathetic vagus nerve on the SA and AV nodes. The heart generally operates at a resting vagus tone, meaning that the vagus nerve is constantly stimulating the SA node, preventing the cardiac cells unstable membrane potential from reaching their threshold as quickly. Decreasing this stimulation will accelerate the depolarisation of the SA, resulting in a faster heartbeat. The sympathetic nerves use norandrenaline to increase the rate of depolarisation of the entire heart. Both these systems activate in response to impulses from the brain.
Changing stroke volume can also affect cardiac output. The greater the EDV that higher stroke volume becomes. This is an adaptive system that depends on the contractility of the heart. In their resting state cardiac myocytes have a large amount of cross over between the actin and myosin filaments, meaning that any contraction does not produce an optimum force. When EDV increases, the heart stretches to accommodate the extra volume, reducing this cross-over, which allows a greater contractile force. Thus more blood coming into the heart will result in an increased output. This is called the Frank-Starling Law of the heart.
Contractility can also be changed by sympathetic stimulation, mostly by noradrenaline. The noradrenaline acts via cellular transduction, to increase the amount of extra-cellular calcium entering the myocytes, allowing more cross-bridge links to be made. This can occur because there is usually not enough calcium to activate all the filaments in the sarcomere.
Arterial pressure can also affect the output as greater pressure in the arteries requires a greater contractile force to pump the same volume of blood against it. This is called afterload.
Myocardial Oxygen Consumption:
The cardiac cells have a limited ability to undergo anaerobic respiration, and a great need to regenerate ATP so a large oxygen need is generated. Roughly 75% of ATP is used in heart contraction, with the other 25% used in cellular transport (i.e. K+/Na+-ATPase). This means that with increased heart contractions, myocardial oxygen consumption goes up to compensate the increased use of ATP. Without the ATP the heart can no longer function. Factors that affect this consumption are largely the same as those that affect cardiac output. That is heart rate (more contractions per unit time), contractility, tension, afterload and preload (determined by EDV).
References: MED2031 Lecture Notes, 2007 Saladin, Anatomy & Physiology: The Unity of Form and Function, McGraw Hill, 2006
CAUSES OF AORTIC STENOSIS: 1. Congenital: Bicuspid aortic valve is the most common cause of aortic stenosis in patients under age 65. About 2% of people are born with aortic valves that have only 2 cusps (bicuspid valves). Although bicuspid valves usually do not impede blood flow when the patients are young, they do not open as widely as normal valves with 3 cusps. Therefore, blood flow across the bicuspid valves is more turbulent, causing increased wear and tear on the valve leaflets. Over time, excessive wear and tear leads to calcification, scarring, and reduced mobility of the valve leaflets. About 10% of bicuspid valves become significantly narrowed, resulting in the symptoms and heart problems of aortic stenosis. 2. Calcific valvular disease (Age related): The most common cause of aortic stenosis in patients 65 years and over is called "senile calcific aortic stenosis." With aging, protein collagen of the valve leaflets is destroyed, and calcium is deposited on the leaflets. Once valve leaflet mobility is reduced by calcification, turbulence across the valve increases, causing scarring, thickening, and stenosis of the valve. Why this aging process progresses to cause significant aortic stenosis in some patients but not in others is not known. 3. Rheumatic fever: a condition resulting from untreated infection by group A streptococcal bacteria. This is thought to develop because of an auto immune reaction triggered by molecular mimicry between the cell wall M proteins of the infecting strep pyogenes and cardiac myosin and laminin. Damage to valve leaflets from rheumatic fever causes increased turbulence across the valve and more damage. The narrowing from rheumatic fever occurs from the fusion (melting together) of the edges (commissures) of the valve leaflets
Also known as aortic valve stenosis, it is a condition in which the narrowing of the aortic valve. This prevents the valve from opening properly and obstructs the flow of blood from the left ventricle to the aorta. Hence blood flow to the rest of the body may be reduced. http://www.nlm.nih.gov/medlineplus/ency/imagepages/18075.htm
A normal Wiggers Diagram can be found in Saladin's Anatomy and Physiology, 3rd edition, Fig19.19.
In Aortic Stenosis, the ventricular pressure and the aortic pressure increases. This can be relected on the Wiggers Diagram like this: http://en.wikipedia.org/wiki/Image:Aortic_Stenosis_-_Hemodynamic_Pressure_Tracing.png
A fourth heart sound can be detected before the first heart sound.
The QRS complex of the ECG takes a longer time and peaks higher due to the left ventricle undergoing hypertrophy.
References Saladin, Anatomy & Physiology: The Unity of Form and Function, McGraw Hill, 2006 http://en.wikipedia.org/wiki/Aortic_stenosis
The heart needs an abundant supply of oxygen and nutrients to function continuously. It is not significantly nourished by blood flowing though it and lies on coronary circulation which supplies the myocardium and epicardium with 250mL/minute of blood.
The two main branches of coronary circulation arise as the aorta leaves the left ventricle. The left and right coronary arteries begin at the aortic sinus (formed by the cusps of the aortic valve).
The left coronary artery passes under the left auricle and divides into two main branches:
The anterior interventricular branch (also called the left anterior descending, LAD) which travels down the anterior interventricular sulcus towards the apex and issues smaller branches to the interventricular septum and anterior walls of both ventricles.
The circumflex artery continues around to the left and runs in the coronary sulcus (also called the atrioventricular groove) and supplies the left atrium and posterior wall of left ventricle/
The right coronary artery supplies the right atrium then continues along the coronary sulcus under the right auricle and gives off two branches.
The marginal artery which supplies the lateral aspect of the right atrium and right ventricle.
The posterior interventricular artery which runs in the posterior interventricular sulcus and supplies the posterior walls of the ventricles. The PIA can sometimes be given off by the left coronary artery (in 33% of people), this is called left dominance, when it is given off by the RCA the heart is said to be right dominant.
Two important anastomoses in coronary circulation: Anterior interventricular with posterior interventricular Right coronary with circumflex
In patients with aortic stenosis, symptoms are a good index of severity. Asymptomatic patients with mild to moderate aortic valve stenosis should be under regular review for assessment and echocardiography. All symptomatic patients should have aortic valve replacement.
Medication: No medication can eliminate aortic valve stenosis. Certain medications can be prescribed to control heart rhythm disturbances associated with AS. Antibiotic prophylaxis treatment before any dental or medical procedures is essential to reduce risk of infective endocarditis.
Surgery: Surgery is the primary treatment for aortic valve stenosis. Surgical procedures to treat aortic valve stenosis include: 1)Aortic valve replacement This is by far the most common surgical treatment for aortic valve stenosis. Surgeons remove the narrowed aortic valve and replace it with a mechanical valve or a tissue valve from a pig, cow or human-cadaver donor. Mechanical valves are made from metal and are durable, but they carry the risk of blood clots forming near the valve and anticoagulant medication must be taken for life. Tissue valves, such as those from a pig, cow or human cadaver, rarely raise risk of blood clots, but they tend to wear out faster than mechanical valves. Another type of tissue valve replacement is autograft, in which the pulmonary valve is used to replace the aortic valve. Replacement of the aortic valve involves open-heart surgery, performed under general anesthesia. Through an incision the length of the breastbone (sternum), the heart is exposed and connected to a heart-lung machine that assumes breathing and blood circulation functions during the procedure. The narrowed aortic valve is then replaced. 2)Aortic valve repair Occasionally, repairing the aortic valve is an option for infants are born with an aortic valve in which the leaflets of the valve are fused together. Doctors can often improve the function of the valve with balloon valvuloplasty to increase the aortic valve opening. This procedure can be done as part of a cardiac catheterization and doesn't require open-heart surgery. In rare cases a surgeon may operate on the valve and separate these leaflets in a procedure called valvotomy, to reduce stenosis and improve blood flow. Or valve repair may involve removing calcium deposits on or near the valve. This helps clear the valve passageway. 3)Balloon valvuloplasty This procedure uses a soft, thin tube (catheter) tipped with a balloon to open up the aortic valve passageway. A balloon is inflated and pushes open the aortic valve, stretching the valve opening. Balloon valvuloplasty may relieve aortic valve stenosis and its symptoms in infants and children. However, in adults, the procedure is not usually successful, and the valve tends to narrow again after initial success. For these reasons, doctors rarely use balloon valvuloplasty today to treat aortic valve stenosis in adults. Aortic valve stenosis can be treated effectively through valve replacement. However, there is still risk of irregular heart rhythms even after the procedure.
*Normal Wiggers Diagram* Wiggers diagram is a standard diagram used in cardiac physiology. It shows the different stages of the cardiac cycle and the effect they have on certain cardiac related variables. Since all the events represented are causally related they can be derived from each other.
X-axis: time Y-axis (usually a combination of): • Blood pressure o Aortic pressure o Ventricular pressure o Atrial pressure • Electrocardiogram • Ventricular volume • Heart sound
*Normal Wiggers Diagram consists of: (Using figure 4A from http://omaha.physiology.arizona.edu/Physiology485/Gore/Lecture10/HeartPump.htm) • Normal ECG reading • Atrial contraction during filling phase in response to the P wave • Increasing ventricular pressure during the isovolumetric contraction phase, beginning with the peak of the QRS complex and the first heart sound as AV valves close • Ejection phase where ventricle pressure rises above aortic pressure causing semilunar valves to open and ventricular volume to decrease • Isovolumetric relaxation phase where ventricle pressure again falls below the aortic pressure and the semilunar valves shut corresponding to second heart sound • Filling phase commences again (first passive then active) in response to the repolarization T wave where atrial pressure again overtakes ventricle pressure and the tricuspid and bicuspid valves open to allow refilling of the ventricles - hence the increase in ventricular volume
*Resources Saladin – Anatomy and Physiology Third Edition http://en.wikipedia.org/wiki/Wiggers_diagram http://sprojects.mmi.mcgill.ca/cardiophysio/EKGwiggers.htm http://omaha.physiology.arizona.edu/Physiology485/Gore/Lecture10/HeartPump.html
Thursday, 8 March 2007 incidence+investigations Incidence of Aortic stenosis: Approximately 2% of people over the age of 65, 3% of people over age 75, and 4% percent of people over age 85 have the disorder. (I would assume these figures are indicative of the developed world, in particular Europe and North America, rather than the developing world).
Investigations for Tom with Aortic Stenosis: ECG: Due to increased pressure generated by the left ventricle, the myocardium muscle of the left ventricle undergoes hypertrophy. It is possible to note left ventricular hypertrophy on an ECG. Signs to note: -tall R wave in lead V5 or V6 (anterior and lateral walls of left ventricle) -deep S wave in lead V1 or V2 (looking at the right ventricle) -inverted t waves in leads I, II, V5 and V6 (anterior and lateral walls of left ventricle) Stress ECG: A stress ECG tests the exercise of your heart. The electrical activity of the heart is measured whilst walking/running on a treadmill or riding a stationary bike. A stress test is performed to determine causes of chest pain, to determine the exercise capacity of the heart , to determine appropriate exercise levels in those initiating an exercise program, and to identify rhythm disturbances during exercise. This test may help to show results of Tom’s fitness capacity and may show any rhythm disturbances. However, in Tom’s case, a normal ECG would adequately and more appropriately show results and signs of aortic stenosis. Echocardiogram: An echocardiogram is an ultrasound on the heart that uses sound waves to produce a picture of the heart. For a person with aortic stenosis, an echocardiogram may show thickened, calcified and immobile aortic valve cusps. Left ventricular hypertrophy may also be seen. Chest X-Ray: A chest X-Ray usually shows a small heart with a prominent, dilated, ascending aorta. This occurs because there is turbulent blood flow above the stenosed aortic valve and produces 'post-stenotic dilation'. Cardiac catheterization: catheters are used to document the systolic pressure difference between the aorta and the left ventricle and to assess left ventricular function. This is an invasive procedure and rarely used now since a large amount of information can be gained from the use of an echocardiogram. Blood tests: Cholesterol: generally not used to monitor or diagnose a disease but used to estimate the risk of developing heart disease, including aortic stenosis. Blood sugar: generally used to test for and diagnose diabetes which may affect peripheral circulation and in turn heart disease may develop. Cardiac Enzymes: used to test for myocardial infarction. Probably not relevant in Tom’s case. Angiogram: A medical imaging technique in which an X-ray picture is taken to visualize the inner opening of blood filled structures, including arteries, veins and the heart chambers. A catheter is usually inserted into the femoral artery and fed along to the desired site in the heart. A radiocontrast agent is administered to make the angiography visualization possible. It is generally used to visualize the blood in the coronary arteries and probably wouldn’t be relevant in Tom’s case.
References: Kumar and Clark, "aortic stenosis", pp. 822-24 ECG made easy, by John R. Hampton, sixth edition, pgs. 93-95, Stress ECG: http://www.umm.edu/ency/article/003878.htm Blood sugar tests: http://www.mayoclinic.com/health/blood-sugar/SA00102 Wikipedia: “Aortic stenosis”, “angiogram”
Is an inflammatory disease that mainly affects children between the ages 5 and 15. The disease is more widespread in less developed countries as a result of poorer hygene and less availability of antibiotic treatment.
If the initial group A strep. infection is untreated it can lead to complications involving the heart, particularly heart valves, skin, joints and the central nervous system.
Why does Rheumatic fever affect the heart?
Damage to the heart is not due to a direct bacterial infection or the production af a toxin. Rather it is thought to be caused by an auto-immune reaction. The antibodies made by the immune system to fight the initial strep infection also react with similar cardiac muscle cell proteins and arterial smooth muscle proteins.
This may affect all three layers of the heart and cause legions with necrotic tissue, mainly in the left ventricle and on the mitral and aortic valves. More than 50% of People who suffer acure Rheumatic fever with carditis* develop chronic valve problems.
• Angina is brought on by coronary artery ischaemia (not enough ischaemia however, for it to cause necrosis) (Not enough blood through the coronary arteries deprives the myocardium of vital oxygen and leads to a build-up of waste products) • This explains why angina can be felt upon physical exertion when ischaemia is exacerbated by a need for more blood to the harder working heart • As blood supply for the coronary arteries comes directly from the aorta just above the aortic valve, stenosis of the valve (narrowing) decreases supply to the coronary arteries thus causing chest pain (angina) • It must also be noted that aortic valve stenosis, forcing the heart to work harder, can cause left ventricular hypertrophy, which can lead to the enlarged heart physically pressing on nerve fibres (phrenic nerve etc.) hence this may also be the cause of angina
Pathophysiology: how does ischaemic tissue cause pain?
• Myocardium deprived of oxygen reverts to anaerobic fermentation to produce its energy for contractions • leads to a build-up of lactic acid (glucose 2 pyruvate lactate + CO2, NADH NAD+, produces 4ATP total) • lactic acid stimulates pain receptors
Sources: Yahoo health: http://health.yahoo.com/topic/heart/resources/article/healthwise/uf4496abc Saladin: Anatomy and Physiology, third edition, 2006 Lectures from the week: Tissue infarction and tissue repair etc.
-Infection, specifically - Infective encocarditis; Recurrent Rheumatic Carditis (if valve lesion has a rheumatic aetiology) -Calcific Embolization – non-mechanical valves develop calcium deposits over time, which could hamper the function of the valve or break off into emboli. -Conduction defects – damage to the AV node/Bundle of His -Sudden heart failure, e.g. upon exertion too soon after surgery -Consequences associated with lifelong use of warfarin (oral anticoagulant) after surgery, e.g. possible haemorrhage, skin necrosis, purpura (bleeding under skin), liver damage, vomiting, diarrhoea. Increasing age and Left Ventricular systolic dysfunction are risk factors for mortality during surgery; otherwise, the risk is less than 5% for patients with normal LV function.
PROGNOSIS of untreated aortic stenosis:
Studies suggest the valve area may decline .1- 0.3 cm squared per year while the systolic pressure gradient may increase by as much as 10-15 mmHg per year.
-Patients with mild Aortic Stenosis can usually lead a normal life. -Patients with severe AS may be asymptomatic for many years; they have an excellent prognosis as only 4% of sudden cardiac deaths from AS are in asymptomatic patients. -After appearance of symptoms, there is a rapid downhill course. Onset of angina and syncope associated with an average survival of 2-3 years if untreated.
References:
http://www.emedicine.com/med/topic157.htm Medical Pharmacology – Aminur Rahman (Vision Publication,2000)
13 comments:
Cardiac Output:
Cardiac output is a measure of the volume of blood pumped by the heart within a particular timeframe (normally measured in L/min). It is calculated by CO = Stroke volume x Heart rate, where the stroke volume gives the volume pumped per beat, and heart rate gives the beats per minute. Cardiac output is not a constant figure and changes depending on a number of variables, most notably venous return (volume of blood returning to the heart) which determines the end-diastolic volume of the heart (volume of blood after contraction of the atria results in the filling of the ventricles).
Changing Heart Rate will change the cardiac output. Heart rate commonly increases in response to exertion or emotional stress. The change is effected by either an increase in sympathetic stimulation of the heart, or a decrease in stimulation by the parasympathetic vagus nerve on the SA and AV nodes. The heart generally operates at a resting vagus tone, meaning that the vagus nerve is constantly stimulating the SA node, preventing the cardiac cells unstable membrane potential from reaching their threshold as quickly. Decreasing this stimulation will accelerate the depolarisation of the SA, resulting in a faster heartbeat. The sympathetic nerves use norandrenaline to increase the rate of depolarisation of the entire heart. Both these systems activate in response to impulses from the brain.
Changing stroke volume can also affect cardiac output. The greater the EDV that higher stroke volume becomes. This is an adaptive system that depends on the contractility of the heart. In their resting state cardiac myocytes have a large amount of cross over between the actin and myosin filaments, meaning that any contraction does not produce an optimum force. When EDV increases, the heart stretches to accommodate the extra volume, reducing this cross-over, which allows a greater contractile force. Thus more blood coming into the heart will result in an increased output. This is called the Frank-Starling Law of the heart.
Contractility can also be changed by sympathetic stimulation, mostly by noradrenaline. The noradrenaline acts via cellular transduction, to increase the amount of extra-cellular calcium entering the myocytes, allowing more cross-bridge links to be made. This can occur because there is usually not enough calcium to activate all the filaments in the sarcomere.
Arterial pressure can also affect the output as greater pressure in the arteries requires a greater contractile force to pump the same volume of blood against it. This is called afterload.
Myocardial Oxygen Consumption:
The cardiac cells have a limited ability to undergo anaerobic respiration, and a great need to regenerate ATP so a large oxygen need is generated. Roughly 75% of ATP is used in heart contraction, with the other 25% used in cellular transport (i.e. K+/Na+-ATPase). This means that with increased heart contractions, myocardial oxygen consumption goes up to compensate the increased use of ATP. Without the ATP the heart can no longer function. Factors that affect this consumption are largely the same as those that affect cardiac output. That is heart rate (more contractions per unit time), contractility, tension, afterload and preload (determined by EDV).
References:
MED2031 Lecture Notes, 2007
Saladin, Anatomy & Physiology: The Unity of Form and Function, McGraw Hill, 2006
Robb
CAUSES OF AORTIC STENOSIS:
1. Congenital: Bicuspid aortic valve is the most common cause of aortic stenosis in patients under age 65. About 2% of people are born with aortic valves that have only 2 cusps (bicuspid valves). Although bicuspid valves usually do not impede blood flow when the patients are young, they do not open as widely as normal valves with 3 cusps. Therefore, blood flow across the bicuspid valves is more turbulent, causing increased wear and tear on the valve leaflets. Over time, excessive wear and tear leads to calcification, scarring, and reduced mobility of the valve leaflets. About 10% of bicuspid valves become significantly narrowed, resulting in the symptoms and heart problems of aortic stenosis.
2. Calcific valvular disease (Age related): The most common cause of aortic stenosis in patients 65 years and over is called "senile calcific aortic stenosis." With aging, protein collagen of the valve leaflets is destroyed, and calcium is deposited on the leaflets. Once valve leaflet mobility is reduced by calcification, turbulence across the valve increases, causing scarring, thickening, and stenosis of the valve. Why this aging process progresses to cause significant aortic stenosis in some patients but not in others is not known.
3. Rheumatic fever: a condition resulting from untreated infection by group A streptococcal bacteria. This is thought to develop because of an auto immune reaction triggered by molecular mimicry between the cell wall M proteins of the infecting strep pyogenes and cardiac myosin and laminin. Damage to valve leaflets from rheumatic fever causes increased turbulence across the valve and more damage. The narrowing from rheumatic fever occurs from the fusion (melting together) of the edges (commissures) of the valve leaflets
http://www.medicinenet.com/aortic_stenosis/page2.htm
DEFINITION: AORTIC STENOSIS
Also known as aortic valve stenosis, it is a condition in which the narrowing of the aortic valve. This prevents the valve from opening properly and obstructs the flow of blood from the left ventricle to the aorta. Hence blood flow to the rest of the body may be reduced.
http://www.nlm.nih.gov/medlineplus/ency/imagepages/18075.htm
See you all on friday!
Jess
Wiggers Diagram - Aortic Stenosis
A normal Wiggers Diagram can be found in Saladin's Anatomy and Physiology, 3rd edition, Fig19.19.
In Aortic Stenosis, the ventricular pressure and the aortic pressure increases. This can be relected on the Wiggers Diagram like this:
http://en.wikipedia.org/wiki/Image:Aortic_Stenosis_-_Hemodynamic_Pressure_Tracing.png
A fourth heart sound can be detected before the first heart sound.
The QRS complex of the ECG takes a longer time and peaks higher due to the left ventricle undergoing hypertrophy.
References
Saladin, Anatomy & Physiology: The Unity of Form and Function, McGraw Hill, 2006
http://en.wikipedia.org/wiki/Aortic_stenosis
Blood Supply To The Heart (Coronary Circulation)
The heart needs an abundant supply of oxygen and nutrients to function continuously.
It is not significantly nourished by blood flowing though it and lies on coronary circulation which supplies the myocardium and epicardium with 250mL/minute of blood.
The two main branches of coronary circulation arise as the aorta leaves the left ventricle. The left and right coronary arteries begin at the aortic sinus (formed by the cusps of the aortic valve).
The left coronary artery passes under the left auricle and divides into two main branches:
The anterior interventricular branch (also called the left anterior descending, LAD) which travels down the anterior interventricular sulcus towards the apex and issues smaller branches to the interventricular septum and anterior walls of both ventricles.
The circumflex artery continues around to the left and runs in the coronary sulcus (also called the atrioventricular groove) and supplies the left atrium and posterior wall of left ventricle/
The right coronary artery supplies the right atrium then continues along the coronary sulcus under the right auricle and gives off two branches.
The marginal artery which supplies the lateral aspect of the right atrium and right ventricle.
The posterior interventricular artery which runs in the posterior interventricular sulcus and supplies the posterior walls of the ventricles.
The PIA can sometimes be given off by the left coronary artery (in 33% of people), this is called left dominance, when it is given off by the RCA the heart is said to be right dominant.
Two important anastomoses in coronary circulation:
Anterior interventricular with posterior interventricular
Right coronary with circumflex
Saladin
Moore and Dalley
MANAGEMENT OF AORTIC STENOSIS
In patients with aortic stenosis, symptoms are a good index of severity. Asymptomatic patients with mild to moderate aortic valve stenosis should be under regular review for assessment and echocardiography. All symptomatic patients should have aortic valve replacement.
Medication:
No medication can eliminate aortic valve stenosis. Certain medications can be prescribed to control heart rhythm disturbances associated with AS. Antibiotic prophylaxis treatment before any dental or medical procedures is essential to reduce risk of infective endocarditis.
Surgery:
Surgery is the primary treatment for aortic valve stenosis. Surgical procedures to treat aortic valve stenosis include:
1)Aortic valve replacement
This is by far the most common surgical treatment for aortic valve stenosis. Surgeons remove the narrowed aortic valve and replace it with a mechanical valve or a tissue valve from a pig, cow or human-cadaver donor. Mechanical valves are made from metal and are durable, but they carry the risk of blood clots forming near the valve and anticoagulant medication must be taken for life. Tissue valves, such as those from a pig, cow or human cadaver, rarely raise risk of blood clots, but they tend to wear out faster than mechanical valves. Another type of tissue valve replacement is autograft, in which the pulmonary valve is used to replace the aortic valve. Replacement of the aortic valve involves open-heart surgery, performed under general anesthesia. Through an incision the length of the breastbone (sternum), the heart is exposed and connected to a heart-lung machine that assumes breathing and blood circulation functions during the procedure. The narrowed aortic valve is then replaced.
2)Aortic valve repair
Occasionally, repairing the aortic valve is an option for infants are born with an aortic valve in which the leaflets of the valve are fused together. Doctors can often improve the function of the valve with balloon valvuloplasty to increase the aortic valve opening. This procedure can be done as part of a cardiac catheterization and doesn't require open-heart surgery. In rare cases a surgeon may operate on the valve and separate these leaflets in a procedure called valvotomy, to reduce stenosis and improve blood flow. Or valve repair may involve removing calcium deposits on or near the valve. This helps clear the valve passageway.
3)Balloon valvuloplasty
This procedure uses a soft, thin tube (catheter) tipped with a balloon to open up the aortic valve passageway. A balloon is inflated and pushes open the aortic valve, stretching the valve opening. Balloon valvuloplasty may relieve aortic valve stenosis and its symptoms in infants and children. However, in adults, the procedure is not usually successful, and the valve tends to narrow again after initial success. For these reasons, doctors rarely use balloon valvuloplasty today to treat aortic valve stenosis in adults.
Aortic valve stenosis can be treated effectively through valve replacement. However, there is still risk of irregular heart rhythms even after the procedure.
Oops.. forgot my references..
Kumar and Clark
http://www.mayoclinic.com/health/aortic-valve-stenosis/DS00418
*Normal Wiggers Diagram*
Wiggers diagram is a standard diagram used in cardiac physiology. It shows the different stages of the cardiac cycle and the effect they have on certain cardiac related variables. Since all the events represented are causally related they can be derived from each other.
X-axis: time
Y-axis (usually a combination of):
• Blood pressure
o Aortic pressure
o Ventricular pressure
o Atrial pressure
• Electrocardiogram
• Ventricular volume
• Heart sound
*Normal Wiggers Diagram consists of:
(Using figure 4A from http://omaha.physiology.arizona.edu/Physiology485/Gore/Lecture10/HeartPump.htm)
• Normal ECG reading
• Atrial contraction during filling phase in response to the P wave
• Increasing ventricular pressure during the isovolumetric contraction phase, beginning with the peak of the QRS complex and the first heart sound as AV valves close
• Ejection phase where ventricle pressure rises above aortic pressure causing semilunar valves to open and ventricular volume to decrease
• Isovolumetric relaxation phase where ventricle pressure again falls below the aortic pressure and the semilunar valves shut corresponding to second heart sound
• Filling phase commences again (first passive then active) in response to the repolarization T wave where atrial pressure again overtakes ventricle pressure and the tricuspid and bicuspid valves open to allow refilling of the ventricles - hence the increase in ventricular volume
*Resources
Saladin – Anatomy and Physiology Third Edition
http://en.wikipedia.org/wiki/Wiggers_diagram
http://sprojects.mmi.mcgill.ca/cardiophysio/EKGwiggers.htm
http://omaha.physiology.arizona.edu/Physiology485/Gore/Lecture10/HeartPump.html
Thursday, 8 March 2007
incidence+investigations
Incidence of Aortic stenosis:
Approximately 2% of people over the age of 65, 3% of people over age 75, and 4% percent of people over age 85 have the disorder.
(I would assume these figures are indicative of the developed world, in particular Europe and North America, rather than the developing world).
Investigations for Tom with Aortic Stenosis:
ECG: Due to increased pressure generated by the left ventricle, the myocardium muscle of the left ventricle undergoes hypertrophy. It is possible to note left ventricular hypertrophy on an ECG. Signs to note:
-tall R wave in lead V5 or V6 (anterior and lateral walls of left ventricle)
-deep S wave in lead V1 or V2 (looking at the right ventricle)
-inverted t waves in leads I, II, V5 and V6 (anterior and lateral walls of left ventricle)
Stress ECG: A stress ECG tests the exercise of your heart. The electrical activity of the heart is measured whilst walking/running on a treadmill or riding a stationary bike. A stress test is performed to determine causes of chest pain, to determine the exercise capacity of the heart , to determine appropriate exercise levels in those initiating an exercise program, and to identify rhythm disturbances during exercise.
This test may help to show results of Tom’s fitness capacity and may show any rhythm disturbances. However, in Tom’s case, a normal ECG would adequately and more appropriately show results and signs of aortic stenosis.
Echocardiogram: An echocardiogram is an ultrasound on the heart that uses sound waves to produce a picture of the heart.
For a person with aortic stenosis, an echocardiogram may show thickened, calcified and immobile aortic valve cusps. Left ventricular hypertrophy may also be seen.
Chest X-Ray: A chest X-Ray usually shows a small heart with a prominent, dilated, ascending aorta. This occurs because there is turbulent blood flow above the stenosed aortic valve and produces 'post-stenotic dilation'.
Cardiac catheterization: catheters are used to document the systolic pressure difference between the aorta and the left ventricle and to assess left ventricular function. This is an invasive procedure and rarely used now since a large amount of information can be gained from the use of an echocardiogram.
Blood tests:
Cholesterol: generally not used to monitor or diagnose a disease but used to estimate the risk of developing heart disease, including aortic stenosis.
Blood sugar: generally used to test for and diagnose diabetes which may affect peripheral circulation and in turn heart disease may develop.
Cardiac Enzymes: used to test for myocardial infarction. Probably not relevant in Tom’s case.
Angiogram: A medical imaging technique in which an X-ray picture is taken to visualize the inner opening of blood filled structures, including arteries, veins and the heart chambers. A catheter is usually inserted into the femoral artery and fed along to the desired site in the heart. A radiocontrast agent is administered to make the angiography visualization possible. It is generally used to visualize the blood in the coronary arteries and probably wouldn’t be relevant in Tom’s case.
References:
Kumar and Clark, "aortic stenosis", pp. 822-24
ECG made easy, by John R. Hampton, sixth edition, pgs. 93-95,
Stress ECG: http://www.umm.edu/ency/article/003878.htm
Blood sugar tests: http://www.mayoclinic.com/health/blood-sugar/SA00102
Wikipedia: “Aortic stenosis”, “angiogram”
Rheumatic Fever:
Is an inflammatory disease that mainly affects children between the ages 5 and 15. The disease is more widespread in less developed countries as a result of poorer hygene and less availability of antibiotic treatment.
If the initial group A strep. infection is untreated it can lead to complications involving the heart, particularly heart valves, skin, joints and the central nervous system.
Why does Rheumatic fever affect the heart?
Damage to the heart is not due to a direct bacterial infection or the production af a toxin. Rather it is thought to be caused by an auto-immune reaction. The antibodies made by the immune system to fight the initial strep infection also react with similar cardiac muscle cell proteins and arterial smooth muscle proteins.
This may affect all three layers of the heart and cause legions with necrotic tissue, mainly in the left ventricle and on the mitral and aortic valves. More than 50% of People who suffer acure Rheumatic fever with carditis* develop chronic valve problems.
Carditis:
- new/changed heart murmurs
- cardiac enlargement
- ECG changes
- Arrhythmias, Heart Block
Alex.
References
Kumar and Clark
Clinical medicine
Angela:
Why does aortic stenosis cause angina?
• Angina is brought on by coronary artery ischaemia (not enough ischaemia however, for it to cause necrosis)
(Not enough blood through the coronary arteries deprives the myocardium of vital oxygen and leads to a build-up of waste products)
• This explains why angina can be felt upon physical exertion when ischaemia is exacerbated by a need for more blood to the harder working heart
• As blood supply for the coronary arteries comes directly from the aorta just above the aortic valve, stenosis of the valve (narrowing) decreases supply to the coronary arteries thus causing chest pain (angina)
• It must also be noted that aortic valve stenosis, forcing the heart to work harder, can cause left ventricular hypertrophy, which can lead to the enlarged heart physically pressing on nerve fibres (phrenic nerve etc.) hence this may also be the cause of angina
Pathophysiology: how does ischaemic tissue cause pain?
• Myocardium deprived of oxygen reverts to anaerobic fermentation to produce its energy for contractions
• leads to a build-up of lactic acid (glucose 2 pyruvate lactate + CO2, NADH NAD+, produces 4ATP total)
• lactic acid stimulates pain receptors
Sources:
Yahoo health:
http://health.yahoo.com/topic/heart/resources/article/healthwise/uf4496abc
Saladin: Anatomy and Physiology, third edition, 2006
Lectures from the week: Tissue infarction and tissue repair etc.
Sorry guys, all those little boxes were arrows....
Ang.
COMPLICATIONS of valve replacement surgery:
-Infection, specifically - Infective encocarditis; Recurrent Rheumatic Carditis (if valve lesion has a rheumatic aetiology)
-Calcific Embolization – non-mechanical valves develop calcium deposits over time, which could hamper the function of the valve or break off into emboli.
-Conduction defects – damage to the AV node/Bundle of His
-Sudden heart failure, e.g. upon exertion too soon after surgery
-Consequences associated with lifelong use of warfarin (oral anticoagulant) after surgery, e.g. possible haemorrhage, skin necrosis, purpura (bleeding under skin), liver damage, vomiting, diarrhoea.
Increasing age and Left Ventricular systolic dysfunction are risk factors for mortality during surgery; otherwise, the risk is less than 5% for patients with normal LV function.
PROGNOSIS of untreated aortic stenosis:
Studies suggest the valve area may decline .1- 0.3 cm squared per year while the systolic pressure gradient may increase by as much as 10-15 mmHg per year.
-Patients with mild Aortic Stenosis can usually lead a normal life.
-Patients with severe AS may be asymptomatic for many years; they have an excellent prognosis as only 4% of sudden cardiac deaths from AS are in asymptomatic patients.
-After appearance of symptoms, there is a rapid downhill course. Onset of angina and syncope associated with an average survival of 2-3 years if untreated.
References:
http://www.emedicine.com/med/topic157.htm
Medical Pharmacology – Aminur Rahman (Vision Publication,2000)
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