An aortic aneurysm is a localized dilation of the aorta that is at least 50% larger than normal. Risk factors include smoking, family history, and conditions like Marfan syndrome. Aneurysms are classified by location (abdominal, thoracic) and shape (fusiform, saccular). Diagnosis involves imaging like ultrasound, CT, or MRI to measure size. Treatment depends on size and growth rate, and may involve surgery if the risk of rupture increases. Medical management focuses on risk factor modification through smoking cessation, blood pressure control, and statin therapy.
1. Echocardiography is the standard method for evaluating the severity of aortic stenosis. The primary parameters used are peak transvalvular velocity, mean transvalvular gradient, and valve area calculated by the continuity equation.
2. Echocardiography plays a major role in evaluating mitral stenosis by allowing confirmation of diagnosis, quantification of stenosis severity, and analysis of valve anatomy. Key indices of severity include pressure gradient, mitral valve area measured by planimetry, and pressure half-time.
3. Guidelines are provided for standardized data collection and measurement techniques for assessing aortic and mitral valve stenosis severity, including recommendations for primary and secondary parameters to measure based on clinical use.
An aortic aneurysm is a dilation of the aorta wall at a weak point. The most common type is abdominal aortic aneurysm, which affects older males. Risk factors include atherosclerosis and smoking. Small aneurysms are monitored while larger aneurysms require surgery to replace the damaged segment. Aortic dissection occurs when blood tears the inner aortic layers, creating a false passageway. It is a medical emergency often presenting with severe chest pain and requires treatment to reduce blood pressure and prevent rupture. Both conditions carry risk of fatal hemorrhage and require lifelong monitoring.
Three sentences:
The document provides details on the anatomy and evaluation of aortic stenosis using echocardiography. It describes the normal aortic valve anatomy and how various types of aortic stenosis like calcific, rheumatic, bicuspid and subvalvular present on echo. Quantitative assessment of aortic stenosis severity is done using Doppler ultrasound to measure the maximum jet velocity and calculate the pressure gradient across the stenotic valve.
The mitral valve lies between the left atrium and left ventricle. Mitral stenosis is usually caused by rheumatic fever which causes scarring of the mitral valve leaflets and commissures. In early mitral stenosis, the leaflets can open but have restricted motion. Over time, the leaflets become thickened and rigid, reducing valve opening. This causes symptoms like dyspnea and pulmonary hypertension. On examination, findings may include an irregular pulse from atrial fibrillation, elevated jugular venous pressure, accentuated S1, and a diastolic murmur. Severe mitral stenosis can lead to right heart failure and complications like hemoptysis.
This document discusses the use of echocardiography in evaluating various types of cardiomyopathies. It provides echocardiographic features of dilated cardiomyopathy including dilated chambers, normal wall thickness, and complications like mitral regurgitation. Hypertrophic cardiomyopathy features include unexplained hypertrophy, diastolic dysfunction, and left ventricular outflow tract obstruction. Restrictive cardiomyopathies show hypertrophy, enlarged atria, restricted filling, and elevated pressures. Left ventricular non-compaction and arrhythmogenic right ventricular cardiomyopathy also have distinct echocardiographic characteristics described.
Noncompaction cardiomyopathy is a rare congenital heart condition caused by the failure of the heart muscle to develop and thicken normally during fetal development. It results in a thickened heart muscle with prominent trabeculations and deep recesses.
The diagnosis is challenging due to a lack of consensus on diagnostic criteria and the inability to clearly differentiate between normal trabeculations and pathological noncompaction using imaging modalities like echocardiography and MRI. Current echocardiographic criteria may be too sensitive, leading to overdiagnosis.
The condition can cause heart failure, arrhythmias and blood clots. Treatment involves medications and lifestyle changes to manage symptoms. The long term prognosis depends on the extent of involvement
Electrical mapping of the heart is a medical procedure that is use to diagnose Arrhythmias in patients. This is done by using sensitive catheter to map the electrical activity in the chambers of the heart.
To begin an electrical mapping procedure, a thin tube called a catheter sheath is inserted into a small incision in the arm or upper thigh. This process is usually visualized using x-rays and a special dye that helps reveal the arteries (called angiography). This catheter is carefully guided through the blood vessels until it is inside the heart.
The document discusses various diseases of the aorta including aortic dissection, intramural hematoma, penetrating atherosclerotic ulcer, aortic aneurysm, atherosclerotic disease, coarctation, and aortic trauma. It provides an overview of the anatomy, clinical presentation, diagnostic imaging, complications, and treatment options for each condition. Key imaging modalities for diagnosis include transthoracic echocardiography, transesophageal echocardiography, CT, and MRI. Mortality rates and predictors of outcome are also reviewed.
1. Echocardiography is the standard method for evaluating the severity of aortic stenosis. The primary parameters used are peak transvalvular velocity, mean transvalvular gradient, and valve area calculated by the continuity equation.
2. Echocardiography plays a major role in evaluating mitral stenosis by allowing confirmation of diagnosis, quantification of stenosis severity, and analysis of valve anatomy. Key indices of severity include pressure gradient, mitral valve area measured by planimetry, and pressure half-time.
3. Guidelines are provided for standardized data collection and measurement techniques for assessing aortic and mitral valve stenosis severity, including recommendations for primary and secondary parameters to measure based on clinical use.
An aortic aneurysm is a dilation of the aorta wall at a weak point. The most common type is abdominal aortic aneurysm, which affects older males. Risk factors include atherosclerosis and smoking. Small aneurysms are monitored while larger aneurysms require surgery to replace the damaged segment. Aortic dissection occurs when blood tears the inner aortic layers, creating a false passageway. It is a medical emergency often presenting with severe chest pain and requires treatment to reduce blood pressure and prevent rupture. Both conditions carry risk of fatal hemorrhage and require lifelong monitoring.
Three sentences:
The document provides details on the anatomy and evaluation of aortic stenosis using echocardiography. It describes the normal aortic valve anatomy and how various types of aortic stenosis like calcific, rheumatic, bicuspid and subvalvular present on echo. Quantitative assessment of aortic stenosis severity is done using Doppler ultrasound to measure the maximum jet velocity and calculate the pressure gradient across the stenotic valve.
The mitral valve lies between the left atrium and left ventricle. Mitral stenosis is usually caused by rheumatic fever which causes scarring of the mitral valve leaflets and commissures. In early mitral stenosis, the leaflets can open but have restricted motion. Over time, the leaflets become thickened and rigid, reducing valve opening. This causes symptoms like dyspnea and pulmonary hypertension. On examination, findings may include an irregular pulse from atrial fibrillation, elevated jugular venous pressure, accentuated S1, and a diastolic murmur. Severe mitral stenosis can lead to right heart failure and complications like hemoptysis.
This document discusses the use of echocardiography in evaluating various types of cardiomyopathies. It provides echocardiographic features of dilated cardiomyopathy including dilated chambers, normal wall thickness, and complications like mitral regurgitation. Hypertrophic cardiomyopathy features include unexplained hypertrophy, diastolic dysfunction, and left ventricular outflow tract obstruction. Restrictive cardiomyopathies show hypertrophy, enlarged atria, restricted filling, and elevated pressures. Left ventricular non-compaction and arrhythmogenic right ventricular cardiomyopathy also have distinct echocardiographic characteristics described.
Noncompaction cardiomyopathy is a rare congenital heart condition caused by the failure of the heart muscle to develop and thicken normally during fetal development. It results in a thickened heart muscle with prominent trabeculations and deep recesses.
The diagnosis is challenging due to a lack of consensus on diagnostic criteria and the inability to clearly differentiate between normal trabeculations and pathological noncompaction using imaging modalities like echocardiography and MRI. Current echocardiographic criteria may be too sensitive, leading to overdiagnosis.
The condition can cause heart failure, arrhythmias and blood clots. Treatment involves medications and lifestyle changes to manage symptoms. The long term prognosis depends on the extent of involvement
Electrical mapping of the heart is a medical procedure that is use to diagnose Arrhythmias in patients. This is done by using sensitive catheter to map the electrical activity in the chambers of the heart.
To begin an electrical mapping procedure, a thin tube called a catheter sheath is inserted into a small incision in the arm or upper thigh. This process is usually visualized using x-rays and a special dye that helps reveal the arteries (called angiography). This catheter is carefully guided through the blood vessels until it is inside the heart.
The document discusses various diseases of the aorta including aortic dissection, intramural hematoma, penetrating atherosclerotic ulcer, aortic aneurysm, atherosclerotic disease, coarctation, and aortic trauma. It provides an overview of the anatomy, clinical presentation, diagnostic imaging, complications, and treatment options for each condition. Key imaging modalities for diagnosis include transthoracic echocardiography, transesophageal echocardiography, CT, and MRI. Mortality rates and predictors of outcome are also reviewed.
The document discusses the physiology of coronary blood flow and the microcirculation. Some key points include:
- Coronary blood flow is determined not only by proximal pressures but also by active compression and decompression of the microcirculation.
- Distal coronary pressure is influenced by both pressure transmitted from the aorta and pressure arising from the microcirculation.
- Fractional flow reserve (FFR) provides a measure of maximum achievable blood flow through a stenosis compared to a normal artery, indicating the functional significance of the stenosis.
- An FFR below 0.80 accurately identifies lesions causing ischemia, while a value above 0.80 reliably excludes ischemia.
Mitral stenosis can be evaluated using echocardiography. Key findings include measuring the mitral valve area using planimetry, pressure half-time, and continuity equation methods. Pressure gradients and pulmonary artery systolic pressure can also assess severity. Mild mitral stenosis is defined as a mitral valve area greater than 1.5 cm2, moderate as 1-1.5 cm2, and severe as less than 1 cm2. Stress echocardiography may reveal symptoms in borderline cases by monitoring pressures with exercise.
This document discusses mitral stenosis, including its etiology, assessment of severity, and role of echocardiography. It provides details on:
- Rheumatic fever is the most common cause of mitral stenosis.
- Echocardiography is used to determine etiology, severity, consequences, and guide treatment decisions. Methods include 2D, Doppler, and exercise echocardiography.
- Severity is assessed by methods like planimetry, pressure gradients, and pressure half-time, with each method having strengths and limitations.
- Consequences of severe mitral stenosis include atrial fibrillation, pulmonary hypertension, and heart failure. Scores like Wilkin's are used to
The document discusses diseases of the aorta, including congenital anomalies, aortic aneurysms, and aortic dissections. It describes the structure and function of the aorta and risk factors for diseases like smoking and hypertension. Symptoms, investigations, and treatments are outlined for different aortic conditions such as thoracic and abdominal aortic aneurysms. Surgical and endovascular repair options are discussed for larger aneurysms at higher risk of rupture.
This document provides an overview of echocardiographic assessment of mitral regurgitation. It describes the anatomy of the mitral valve including the leaflets, annulus, chordae, and papillary muscles. It discusses Carpentier's functional classification system for describing the mechanism of mitral valve dysfunction. Methods for assessing severity are covered, including color flow imaging, continuous wave Doppler, vena contracta width, proximal isovelocity surface area, and volumetric assessment. Key points are made about evaluating jet direction, duration, and velocity in context of blood pressure. The importance of assessing left ventricular and left atrial size and function is also highlighted.
This document discusses bicuspid aortic valve (BAV), including its pathogenesis, diagnosis, natural history, and management. Key points include:
- BAV has a genetic component and is associated with accelerated aortic valve disease and aortopathy.
- Diagnosis is typically by echocardiogram which can identify the raphe and systolic doming. MRI/CT may be needed if unclear on echo.
- Complications include aortic stenosis, aortic regurgitation, endocarditis, and aortic aneurysm/dissection. Progression is often faster than tricuspid valves.
- Management involves surveillance of the aorta size and valve function. Surgery is recommended
This document summarizes the echocardiographic assessment of mitral stenosis (MS). It describes the anatomy of the mitral valve and causes of MS. Methods for assessing MS severity include measuring the pressure gradient, mitral valve area using planimetry and pressure half-time, and pulmonary artery pressure. Suitability for percutaneous transvenous mitral commissurotomy is evaluated. Concomitant valve lesions are also identified. Stress echocardiography may be used when symptoms are equivocal. Transesophageal echocardiography is recommended in some cases.
The aortic root consists of the aortic annulus, sinuses of Valsalva, and sinotubular junction. It provides support for the aortic valve leaflets and connects the left ventricle to the ascending aorta. Abnormalities of the aortic root can cause aortic insufficiency. Surgical techniques for addressing aortic root pathology include replacement using a valve conduit or autograft, as well as techniques to enlarge the annulus such as the Nicks and Manouguian procedures. The choice of technique depends on factors like patient age and anatomy.
This document describes procedures for aortic valve replacement and repair. It discusses excising the native aortic valve and implanting a prosthetic valve using sutures placed around the annulus. For small annuli, the aortic root can be enlarged using techniques like the Nicks-Nunez or Konno-Rastan methods which involve patching the aortic wall. The document also outlines techniques for reconstructing valves, including patching leaflet perforations or tears.
This document summarizes surgical techniques for treating aortic arch aneurysms presented by Dr. Konstadinos Plestis of Lenox Hill Heart and Vascular Institute. It discusses various cerebral protection methods for arch surgery including deep hypothermic circulatory arrest, retrograde cerebral perfusion, and antegrade cerebral perfusion. It also presents case studies of complex arch surgeries including re-do cases and total arch replacements using trifurcated grafts. The summary emphasizes that total arch replacement with trifurcated grafts has improved outcomes by simplifying the technique and that cerebral protection methods have reduced mortality and neurological complications of arch surgery.
This document discusses aortic dissection, including:
1. It provides an introduction defining acute aortic syndromes and the types of aortic dissection.
2. It covers the incidence, risk factors, classifications, pathogenesis, natural history, signs and symptoms, diagnostic testing including imaging and labs, and management approaches for aortic dissection.
3. The management focuses on reducing blood pressure and pulse pressure through beta blockers and other antihypertensive drugs to prevent extension of the dissection.
Fractional flow reserve (FFR) is a technique that evaluates the hemodynamic significance of coronary artery stenoses. It is defined as the ratio of maximal flow achievable in the stenotic coronary artery to the maximal flow achievable if the artery was normal. An FFR value ≤ 0.80 is considered hemodynamically significant. Several clinical trials including DEFER and FAME have found that FFR-guided revascularization reduces major adverse cardiac events compared to angiography-guided procedures alone by helping to identify which intermediate lesions are functionally significant. Guidelines recommend using FFR to guide revascularization decisions, especially for intermediate lesions, multivessel disease, and acute coronary syndromes.
This document discusses cardiac tamponade, which occurs when fluid rapidly accumulates in the pericardial sac, putting pressure on the heart and reducing cardiac function. Key points include:
- Pericardial effusion puts pressure on the heart, causing symptoms like chest pain and shortness of breath.
- Cardiac tamponade occurs when a rapid accumulation of fluid in the pericardial sac severely compresses the heart.
- Echocardiography is useful for diagnosing tamponade by showing findings like pericardial effusion, right ventricular collapse, and reduced respiratory variation in blood flow velocities.
- Tamponade is a medical emergency treated initially with medications and peric
Aortic stenosis is a narrowing of the aortic valve that obstructs blood flow from the left ventricle to the aorta. It can be caused by rheumatic heart disease or congenital issues. As the stenosis progresses, it increases left ventricular pressure and causes compensatory hypertrophy. Symptoms include dyspnea, dizziness, angina, and syncope. On examination, one may hear a crescendo-decrescendo murmur and feel a weak pulse. Echocardiography can measure valve area and gradients to diagnose and classify severity. Treatment options include medical management for symptoms or valve replacement surgery or TAVR for severe cases.
Anatomy of mitral valve echo evaluationmadhusiva03
The document discusses the anatomy and function of the mitral valve complex. It notes that the mitral valve has a triple function regulating blood flow between the left atrium and ventricle. The mitral valve complex relies on normal morphology and function of the annulus, leaflets, chordae tendineae, papillary muscles, and left ventricle. Echocardiography is useful for evaluating each of these structures and identifying abnormalities that can cause mitral dysfunction. Detailed assessment of the leaflet segments, called scallops, aids in characterizing valvular lesions.
This document discusses the Norwood procedure for treating hypoplastic left heart syndrome (HLHS). It begins with an overview of the seminar topics, including the physiology of HLHS, palliative measures, and staged surgical options. It then delves into detailed anatomy and morphology, defining HLHS and discussing major subtypes. The remainder covers clinical presentation, diagnostic testing methods like echocardiography and cardiac catheterization, and historical milestones in HLHS management.
The document discusses atrial septal defects (ASDs), including indications for closure, procedural details, and echocardiographic assessment. Key points include:
- ASD closure is recommended in the presence of right-sided heart volume overload or symptoms. It prevents further deterioration and helps normalize heart size.
- Indications for closure include hemodynamically significant ASD, paradoxical embolism risk, and transient cyanosis. Contraindications include irreversible pulmonary hypertension.
- Echocardiography is used to assess defect size, rims, and shunt severity. Deficient rims, especially aortic and superior vena cava, increase erosion risk post-closure.
The document provides information on aortic valve disease including anatomy, etiology, and pathophysiology. It describes the key components of the aortic root including the aortic annulus, cusps, sinuses, and sinotubular junction. The three main causes of aortic stenosis are discussed as congenital bicuspid valve with calcification, calcification of a normal trileaflet valve, and rheumatic disease. The pathophysiology of aortic stenosis involves left ventricular pressure overload leading to hypertrophy and eventually decreased ejection fraction if severe stenosis is not corrected.
- A 17-year old male collapsed during a basketball game and was diagnosed with NSTEMI. Coronary angiogram revealed anomalous origins of the coronary arteries.
- A 20-year old college student presented with worsening CHF symptoms and exertional chest pain. Angiogram showed anomalous pulmonary origin of the left coronary artery (ALCAPA).
- Coronary artery anomalies are variations in origin, course, or structure that occur in 1-5% of patients. Anomalous origins from the opposite sinus can cause sudden death, especially if the artery courses between the aorta and pulmonary artery. Surgical repair is usually recommended for high-risk anomalies.
This document discusses aortic aneurysms, including their anatomy, physiology, risk factors, diagnosis, and management. It provides details on:
1) The layers of the aortic wall and how they give the aorta elasticity and strength.
2) Factors that cause the aortic wall to stiffen with age like increases in collagen and calcification of elastic fibers.
3) Definitions of aortic aneurysm and classifications based on location and shape. Thoracic aortic aneurysms involve the ascending aorta while abdominal aortic aneurysms are infrarenal.
4) Screening recommendations, diagnosis using imaging like ultrasound, CT and echocardiography, and considerations for open surgical repair
The document discusses the physiology of coronary blood flow and the microcirculation. Some key points include:
- Coronary blood flow is determined not only by proximal pressures but also by active compression and decompression of the microcirculation.
- Distal coronary pressure is influenced by both pressure transmitted from the aorta and pressure arising from the microcirculation.
- Fractional flow reserve (FFR) provides a measure of maximum achievable blood flow through a stenosis compared to a normal artery, indicating the functional significance of the stenosis.
- An FFR below 0.80 accurately identifies lesions causing ischemia, while a value above 0.80 reliably excludes ischemia.
Mitral stenosis can be evaluated using echocardiography. Key findings include measuring the mitral valve area using planimetry, pressure half-time, and continuity equation methods. Pressure gradients and pulmonary artery systolic pressure can also assess severity. Mild mitral stenosis is defined as a mitral valve area greater than 1.5 cm2, moderate as 1-1.5 cm2, and severe as less than 1 cm2. Stress echocardiography may reveal symptoms in borderline cases by monitoring pressures with exercise.
This document discusses mitral stenosis, including its etiology, assessment of severity, and role of echocardiography. It provides details on:
- Rheumatic fever is the most common cause of mitral stenosis.
- Echocardiography is used to determine etiology, severity, consequences, and guide treatment decisions. Methods include 2D, Doppler, and exercise echocardiography.
- Severity is assessed by methods like planimetry, pressure gradients, and pressure half-time, with each method having strengths and limitations.
- Consequences of severe mitral stenosis include atrial fibrillation, pulmonary hypertension, and heart failure. Scores like Wilkin's are used to
The document discusses diseases of the aorta, including congenital anomalies, aortic aneurysms, and aortic dissections. It describes the structure and function of the aorta and risk factors for diseases like smoking and hypertension. Symptoms, investigations, and treatments are outlined for different aortic conditions such as thoracic and abdominal aortic aneurysms. Surgical and endovascular repair options are discussed for larger aneurysms at higher risk of rupture.
This document provides an overview of echocardiographic assessment of mitral regurgitation. It describes the anatomy of the mitral valve including the leaflets, annulus, chordae, and papillary muscles. It discusses Carpentier's functional classification system for describing the mechanism of mitral valve dysfunction. Methods for assessing severity are covered, including color flow imaging, continuous wave Doppler, vena contracta width, proximal isovelocity surface area, and volumetric assessment. Key points are made about evaluating jet direction, duration, and velocity in context of blood pressure. The importance of assessing left ventricular and left atrial size and function is also highlighted.
This document discusses bicuspid aortic valve (BAV), including its pathogenesis, diagnosis, natural history, and management. Key points include:
- BAV has a genetic component and is associated with accelerated aortic valve disease and aortopathy.
- Diagnosis is typically by echocardiogram which can identify the raphe and systolic doming. MRI/CT may be needed if unclear on echo.
- Complications include aortic stenosis, aortic regurgitation, endocarditis, and aortic aneurysm/dissection. Progression is often faster than tricuspid valves.
- Management involves surveillance of the aorta size and valve function. Surgery is recommended
This document summarizes the echocardiographic assessment of mitral stenosis (MS). It describes the anatomy of the mitral valve and causes of MS. Methods for assessing MS severity include measuring the pressure gradient, mitral valve area using planimetry and pressure half-time, and pulmonary artery pressure. Suitability for percutaneous transvenous mitral commissurotomy is evaluated. Concomitant valve lesions are also identified. Stress echocardiography may be used when symptoms are equivocal. Transesophageal echocardiography is recommended in some cases.
The aortic root consists of the aortic annulus, sinuses of Valsalva, and sinotubular junction. It provides support for the aortic valve leaflets and connects the left ventricle to the ascending aorta. Abnormalities of the aortic root can cause aortic insufficiency. Surgical techniques for addressing aortic root pathology include replacement using a valve conduit or autograft, as well as techniques to enlarge the annulus such as the Nicks and Manouguian procedures. The choice of technique depends on factors like patient age and anatomy.
This document describes procedures for aortic valve replacement and repair. It discusses excising the native aortic valve and implanting a prosthetic valve using sutures placed around the annulus. For small annuli, the aortic root can be enlarged using techniques like the Nicks-Nunez or Konno-Rastan methods which involve patching the aortic wall. The document also outlines techniques for reconstructing valves, including patching leaflet perforations or tears.
This document summarizes surgical techniques for treating aortic arch aneurysms presented by Dr. Konstadinos Plestis of Lenox Hill Heart and Vascular Institute. It discusses various cerebral protection methods for arch surgery including deep hypothermic circulatory arrest, retrograde cerebral perfusion, and antegrade cerebral perfusion. It also presents case studies of complex arch surgeries including re-do cases and total arch replacements using trifurcated grafts. The summary emphasizes that total arch replacement with trifurcated grafts has improved outcomes by simplifying the technique and that cerebral protection methods have reduced mortality and neurological complications of arch surgery.
This document discusses aortic dissection, including:
1. It provides an introduction defining acute aortic syndromes and the types of aortic dissection.
2. It covers the incidence, risk factors, classifications, pathogenesis, natural history, signs and symptoms, diagnostic testing including imaging and labs, and management approaches for aortic dissection.
3. The management focuses on reducing blood pressure and pulse pressure through beta blockers and other antihypertensive drugs to prevent extension of the dissection.
Fractional flow reserve (FFR) is a technique that evaluates the hemodynamic significance of coronary artery stenoses. It is defined as the ratio of maximal flow achievable in the stenotic coronary artery to the maximal flow achievable if the artery was normal. An FFR value ≤ 0.80 is considered hemodynamically significant. Several clinical trials including DEFER and FAME have found that FFR-guided revascularization reduces major adverse cardiac events compared to angiography-guided procedures alone by helping to identify which intermediate lesions are functionally significant. Guidelines recommend using FFR to guide revascularization decisions, especially for intermediate lesions, multivessel disease, and acute coronary syndromes.
This document discusses cardiac tamponade, which occurs when fluid rapidly accumulates in the pericardial sac, putting pressure on the heart and reducing cardiac function. Key points include:
- Pericardial effusion puts pressure on the heart, causing symptoms like chest pain and shortness of breath.
- Cardiac tamponade occurs when a rapid accumulation of fluid in the pericardial sac severely compresses the heart.
- Echocardiography is useful for diagnosing tamponade by showing findings like pericardial effusion, right ventricular collapse, and reduced respiratory variation in blood flow velocities.
- Tamponade is a medical emergency treated initially with medications and peric
Aortic stenosis is a narrowing of the aortic valve that obstructs blood flow from the left ventricle to the aorta. It can be caused by rheumatic heart disease or congenital issues. As the stenosis progresses, it increases left ventricular pressure and causes compensatory hypertrophy. Symptoms include dyspnea, dizziness, angina, and syncope. On examination, one may hear a crescendo-decrescendo murmur and feel a weak pulse. Echocardiography can measure valve area and gradients to diagnose and classify severity. Treatment options include medical management for symptoms or valve replacement surgery or TAVR for severe cases.
Anatomy of mitral valve echo evaluationmadhusiva03
The document discusses the anatomy and function of the mitral valve complex. It notes that the mitral valve has a triple function regulating blood flow between the left atrium and ventricle. The mitral valve complex relies on normal morphology and function of the annulus, leaflets, chordae tendineae, papillary muscles, and left ventricle. Echocardiography is useful for evaluating each of these structures and identifying abnormalities that can cause mitral dysfunction. Detailed assessment of the leaflet segments, called scallops, aids in characterizing valvular lesions.
This document discusses the Norwood procedure for treating hypoplastic left heart syndrome (HLHS). It begins with an overview of the seminar topics, including the physiology of HLHS, palliative measures, and staged surgical options. It then delves into detailed anatomy and morphology, defining HLHS and discussing major subtypes. The remainder covers clinical presentation, diagnostic testing methods like echocardiography and cardiac catheterization, and historical milestones in HLHS management.
The document discusses atrial septal defects (ASDs), including indications for closure, procedural details, and echocardiographic assessment. Key points include:
- ASD closure is recommended in the presence of right-sided heart volume overload or symptoms. It prevents further deterioration and helps normalize heart size.
- Indications for closure include hemodynamically significant ASD, paradoxical embolism risk, and transient cyanosis. Contraindications include irreversible pulmonary hypertension.
- Echocardiography is used to assess defect size, rims, and shunt severity. Deficient rims, especially aortic and superior vena cava, increase erosion risk post-closure.
The document provides information on aortic valve disease including anatomy, etiology, and pathophysiology. It describes the key components of the aortic root including the aortic annulus, cusps, sinuses, and sinotubular junction. The three main causes of aortic stenosis are discussed as congenital bicuspid valve with calcification, calcification of a normal trileaflet valve, and rheumatic disease. The pathophysiology of aortic stenosis involves left ventricular pressure overload leading to hypertrophy and eventually decreased ejection fraction if severe stenosis is not corrected.
- A 17-year old male collapsed during a basketball game and was diagnosed with NSTEMI. Coronary angiogram revealed anomalous origins of the coronary arteries.
- A 20-year old college student presented with worsening CHF symptoms and exertional chest pain. Angiogram showed anomalous pulmonary origin of the left coronary artery (ALCAPA).
- Coronary artery anomalies are variations in origin, course, or structure that occur in 1-5% of patients. Anomalous origins from the opposite sinus can cause sudden death, especially if the artery courses between the aorta and pulmonary artery. Surgical repair is usually recommended for high-risk anomalies.
This document discusses aortic aneurysms, including their anatomy, physiology, risk factors, diagnosis, and management. It provides details on:
1) The layers of the aortic wall and how they give the aorta elasticity and strength.
2) Factors that cause the aortic wall to stiffen with age like increases in collagen and calcification of elastic fibers.
3) Definitions of aortic aneurysm and classifications based on location and shape. Thoracic aortic aneurysms involve the ascending aorta while abdominal aortic aneurysms are infrarenal.
4) Screening recommendations, diagnosis using imaging like ultrasound, CT and echocardiography, and considerations for open surgical repair
This document discusses thoracic aortic aneurysms. It defines a thoracic aneurysm and notes their locations in the aorta. While less common than abdominal aortic aneurysms, thoracic aneurysms carry a high mortality. They develop due to degradation of the tunica media layer of the aorta. Risk factors include family history, hypertension, smoking, and advancing age. Symptoms vary depending on the location but often include chest or back pain. Imaging such as CT scan is used to diagnose. Management involves medical therapy as well as surgical intervention depending on the location and size of the aneurysm.
The aorta is prone to several diseases that can lead to significant morbidity and mortality. Diseases such as cystic medial degeneration, atherosclerosis, and inflammation can weaken the aortic wall and cause aneurysm or dissection. Aortic aneurysms are classified based on location in the thoracic or abdominal aorta. Diagnostic imaging can identify aneurysms, which often require surgical repair when they reach a certain size to prevent complications like rupture. Aortic dissection involves splitting of the aortic wall and formation of a false lumen, typically requiring emergent surgery if the ascending aorta is involved.
Aortic Aneurysm: Diagnosis, Management, Exercise Testing, And TrainingJavidsultandar
An aortic aneurysm is a balloon-like bulge in the aorta, the large artery that carries blood from the heart through the chest and torso.
Aortic aneurysms can dissect or rupture:
The force of blood pumping can split the layers of the artery wall, allowing blood to leak in between them. This process is called a dissection.
The aneurysm can burst completely, causing bleeding inside the body. This is called a rupture.
Dissections and ruptures are the cause of most deaths from aortic aneurysms.
PDA is a congenital heart defect where the ductus arteriosus remains open after birth, creating a connection between the pulmonary artery and aorta. This results in a left-to-right shunt, overloading the left heart and lungs. Symptoms range from none to dyspnea, cardiac failure, and pulmonary hypertension. Diagnosis is made through chest X-ray, ECG, echocardiogram and other imaging. Small PDAs may be left untreated if asymptomatic, while larger ones require closure through transcatheter devices, surgery, or medications to relieve symptoms.
AR, or aortic regurgitation, occurs when the aortic valve does not close properly, allowing blood to flow backward into the left ventricle. It can be caused by damage to the aortic valve leaflets or distortion/dilation of the aortic root. In developed countries, the most common causes are aortic root dilation or a congenital bicuspid aortic valve. AR is more common in men than women. Symptomatic patients or asymptomatic patients with reduced ejection fraction or increased left ventricular dimensions require surgical treatment such as aortic valve replacement. The prognosis depends on symptoms and left ventricular function, with asymptomatic patients having normal ejection fraction having an excellent long-term prognosis.
This document provides information on various types of aneurysms, including their classification, risk factors, symptoms, investigations, and management. It discusses thoracoabdominal aneurysms, abdominal aortic aneurysms, and ruptured abdominal aortic aneurysms in particular detail. For abdominal aortic aneurysms, it outlines their prevalence, risk factors like smoking and atherosclerosis, classifications based on location and symptoms, potential complications, and treatments including open surgical repair, endovascular aneurysm repair, and management of ruptured abdominal aortic aneurysms.
1) A 38-year old hypertensive smoker presented with severe central chest pain and was diagnosed with acute aortic dissection.
2) Aortic dissection occurs when a tear in the inner layer of the aorta allows blood to enter and force the layers apart, creating a false lumen. If untreated, mortality is as high as 50% within a week.
3) Diagnosis is made through imaging like CT, MRI, TTE or TEE which can detect the intimal flap separating the true and false lumens. Management involves controlling blood pressure, heart rate and pain to prevent progression while emergent surgery is needed for Type A dissections involving the ascending aorta.
A retired colonel presented to the emergency room with chronic chest pain. Further evaluation revealed he had a massive haemothorax secondary to a ruptured aortic aneurysm. Autopsy showed aortic aneurysms are caused by alterations to the delicate balance in the aortic wall that leads to dilatation. Thoracic aortic aneurysms are generally repaired electively when they reach a diameter of 6 cm or greater to prevent fatal rupture. Treatment options include open surgical repair or endovascular stent graft placement depending on the location and extent of the aneurysm.
Atrial septal defect (ASD) is an abnormal opening in the wall separating the left and right atria of the heart. There are several types of ASDs including secundum, ostium primum, sinus venosus, and coronary sinus defects. ASDs are usually diagnosed through echocardiography which can determine the size and location of the defect. Small, asymptomatic ASDs may not require treatment, but larger defects with evidence of right heart strain often warrant closure either through open heart surgery or a nonsurgical approach using an implantable device delivered through catheters. Both methods effectively close the defect to prevent long-term complications like heart failure and pulmonary hypertension.
Atrial septal defect (ASD) is an abnormal opening in the wall separating the left and right atria of the heart. There are several types of ASDs. Secundum ASDs, which occur in the fossa ovalis, account for 75% of cases. ASDs are usually diagnosed with echocardiography. Small, asymptomatic ASDs may not require treatment, but larger defects can cause heart failure and pulmonary hypertension if left untreated. Larger ASDs are often closed either surgically or non-surgically using devices delivered through catheters. Both methods are generally effective though surgery carries risks of complications.
Cardiac tamponade is a life-threatening condition caused by fluid accumulation in the pericardium that compresses the heart. Echocardiography is important for diagnosing tamponade and guiding treatment. Key echocardiographic signs include chamber collapse, increased ventricular interdependence seen on Doppler imaging, and inferior vena cava plethora. Echocardiography can also guide pericardiocentesis procedures to drain fluid from the pericardium. It is a useful non-invasive tool for both diagnosing and managing cardiac tamponade.
This document summarizes various heart diseases including coronary heart disease, stable angina, acute myocardial infarction, valvular heart diseases, and their appearances on chest radiographs. Coronary artery disease is caused by atherosclerosis and presents as coronary calcification or cardiomyopathy. Acute MI can cause pulmonary edema on CXR. Valvular diseases like aortic stenosis present with left ventricular hypertrophy and calcification while aortic regurgitation causes cardiomegaly. Mitral stenosis presents with left atrial enlargement and pulmonary hypertension.
Adult Congenital Heart Disease can affect over 1 million adults in the US. Common conditions include Atrial Septal Defects, Ventricular Septal Defects, Patent Ductus Arteriosus, Bicuspid Aortic Valve, Coarctation of the Aorta, Tetralogy of Fallot, and Transposition of the Great Arteries. Clinical presentation and treatment depends on the specific condition and degree of severity. Long term monitoring is important for complications. Pregnancy can also pose additional risks for some congenital heart conditions.
Valvular heart disease refers to disorders that affect one of the heart's valves, causing stenosis (narrowing) or regurgitation (leakage). The major types are aortic stenosis, aortic regurgitation, mitral stenosis, mitral regurgitation, tricuspid stenosis, and tricuspid regurgitation. Symptoms depend on the specific valve affected and include shortness of breath, chest pain, fatigue, and heart failure. Diagnosis involves listening for murmurs, ECGs, echocardiograms, and cardiac catheterization. Treatment ranges from medication and lifestyle changes to surgery depending on severity, with valve replacement or repair being done for severe cases.
The document discusses various types of valvular heart disease, including aortic stenosis, aortic regurgitation, mitral stenosis, and mitral regurgitation. It provides details on the causes, symptoms, physical exam findings, diagnostic tests and treatments for each condition. For aortic stenosis, the case describes a 67-year-old male with symptoms of dyspnea and chest pain, who is found to have a systolic thrill and murmur, indicating severe aortic valve stenosis. Diagnostic tests and treatments are outlined for each valvular disease.
This document provides information about a seminar on aortic dissection presented by Monika Devi. It discusses the introduction, types, causes, symptoms, risk factors, diagnosis, treatment, complications and prevention of aortic dissection. The two main types are Type A, which involves the ascending aorta, and Type B, which only involves the descending aorta. Causes include high blood pressure, genetic conditions like Marfan syndrome, and traumatic injury. Symptoms can include chest pain and symptoms of a stroke. Treatment depends on the type but may involve medications to lower blood pressure or surgery to repair the tear in the aorta. Complications can include death, organ damage or stroke if not properly treated.
The document discusses aortic aneurysms, including their anatomy, types, causes, clinical features, diagnosis, and treatment. It defines aortic aneurysm as a localized dilatation of the aorta that is at least 1.5 times the normal diameter. There are two main types - fusiform and saccular. Clinical features may include back pain, abdominal pain, and signs of peripheral vascular disease. Diagnosis involves imaging like CT scans and ultrasound. Treatment depends on location and size, and may include surgery, endovascular stent grafts, or monitoring for smaller aneurysms.
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
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- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
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TEST BANK For An Introduction to Brain and Behavior, 7th Edition by Bryan Kol...rightmanforbloodline
TEST BANK For An Introduction to Brain and Behavior, 7th Edition by Bryan Kolb, Ian Q. Whishaw, Verified Chapters 1 - 16, Complete Newest Versio
TEST BANK For An Introduction to Brain and Behavior, 7th Edition by Bryan Kolb, Ian Q. Whishaw, Verified Chapters 1 - 16, Complete Newest Version
TEST BANK For An Introduction to Brain and Behavior, 7th Edition by Bryan Kolb, Ian Q. Whishaw, Verified Chapters 1 - 16, Complete Newest Version
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Osteoporosis - Definition , Evaluation and Management .pdfJim Jacob Roy
Osteoporosis is an increasing cause of morbidity among the elderly.
In this document , a brief outline of osteoporosis is given , including the risk factors of osteoporosis fractures , the indications for testing bone mineral density and the management of osteoporosis
3. Aortic aneurysm
• Aortic aneurysm is a localized or diffuse dilation of an aorta
with a diameter at least 50% greater than the normal size
of the aorta
• Aneurysm is the second most frequent disease of the aorta
after atherosclerosis
• The strongest predictor of AAA formation is positive family
history
• Smoking is the most important modifiable risk factor in the
formation, progression, and rupture risk of AAA
• The male to female ratio is approximately 2:1, although
women have a higher incidence of aneurysm rupture.
• mean age for diagnosis in sixth decade of life
4. Type
• Abdominal Aortic aneurysm
• Thoracic aneurysms
• Thoraco-Abdominal Aortic aneurysm
•
• 45% of thoracic aneurysms involved the
ascending aorta, 10% the arch, 35% the
descending aorta, and 10% the thoracoabdominal
aorta
5. Classification by shape
Fusiform aneurysms are more common,
associated with atherosclerotic or collagen
vascular disease, and usually affect a longer
segment of the aorta, producing a dilation of the
entire circumference of the vessel wall.
Saccular aneurysms are more localized, confined
to an isolated segment of the aorta, and produce
a localized outpouching of the vessel wall
Aortic arch aneurysms are commonly saccular
Fusiform aneurysms have a higher operative
mortality than saccular aneurysms
7. Risk Factors
– Smoking
– COPD
– HTN
– Male gender
– Older age
– High BMI
– Abnormal aortic valve (e.g., bicuspid valve)
– Family history
8. pathophysiology
• The number of collagen and elastic fibres is reduced
within the aneurysmal segment of the aorta vascular
wall strength is further compromised by several factors
(i) local elastin resorption caused by increased elastase
activity;
(ii) localized wall inflammatory changes;
(iii) increased protease activity;
(iv) mural thrombus formation in the arterial wall and
plasminogen activation
9.
10. Ruptured AAA
Die outside
Hospital
Die In Hospital
Survive with
major
complications
Survive with
minor or no
complication
• Triad of
Abd. or back
pain
Hypotension
Pulsatile
Abd. mass
11. Aortic growth in thoracic aortic
aneurysms
• Familial TAAs grow faster, up to 2.1 mm/year (combined ascending
and descending TAA).
• Syndromic TAA growth rates also vary.
• In patients with Marfan syndrome, the TAA growth is on average at
0.5–1 mm/year, whereas TAAs in patients with Loeys-Dietz
syndrome (LDS) can grow even faster than 10 mm/year, resulting in
death at a mean age of 26 years.
• TAAs of the descending aorta grow faster (at 3 mm/year) than
those in ascending aorta (1 mm/year)
12. Complications of Thoracic
Aortic Aneurysms
• Aortic rupture
• Aortic regurgitation
• Tracheobronchial and esophageal compression
• Right pulmonary artery or right ventricular
outflow tractobstruction
• Systemic embolism from mural thrombus
13. Risk of aortic dissection
• There is a rapid increase in the risk of
dissection or rupture when the aortic
diameter is 60 mm for the ascending aorta
and 70 mm for the descending aorta.
• Although dissection may occur in patients
with a small aorta, the individual risk is very
low
14. In Marfan syndrome, aortic enlargement is
generally maximal at the sinuses of Valsalva,
responsible for annulo-aortic ectasia.
In patients with BAV, three enlargement
patterns are described
Level of the sinuses of Valsalva,
Supracoronary ascending aorta,
The sinotubular junction level (cylindrical
shape).
17. SYMPTOMS
• Most of aortic ANEURSYMS may be clinically silent.
• Anterior chest pain secondary to compression of
• (1) Coronary arteries
• (2) Sensory mediastinal nerves
• Chronic back pain may occur descending aortic aneurysms
• CHF symptoms secondary to aortic annular enlargement
• (1) Widened pulse pressure
• (2) Diastolic murmur
• Facial and upper trunk venous congestion secondary to
superior vena cava compression
• Blood pressure usually elevated chronically
18. Conti .
Acute deep, aching or throbbing chest or abdominal pain that
can spread to the back, buttocks, groin or legs, suggestive
of AD or other AAS, and best described as ‘feeling of
rupture’.
Cough, shortness of breath, or difficult or painful
swallowing in large TAAs.
Constant or intermittent abdominal pain or discomfort, a
pulsating feeling in the abdomen, or feeling of fullness after
minimal food intake in large AAAs.
Stroke, transient ischaemic attack, or claudication
secondary to aortic atherosclerosis.
Hoarseness due to left laryngeal nerve palsy in rapidly
progressing lesions
19. Aortic Aneurysms
Diagnosis
• Arteriography:
– Cannot determine aneurysm size because of mural
thrombus
– Indications for obtaining arteriography
• Suspicion of visceral ischemia
• Occlusive disease of iliac and femoral arteries
• Severe HTN, or impair renal function
• ? Horseshoe Kidney
• Suprarenal of TAAA component
• Femoro-Popliteal Aneurysms
20. CHEST XRAY
• Loss of aortic contour
• Mediastinal widening
• Dilated descending thoracic
aorta,
• aortic calcifications
• upward deviation of the left
mainstem bronchus, and/or
new left pleural effusion.
• Deviation of the trachea to the
right
• Left hemothorax
21. Aortic Aneurysms
Diagnosis
• Ultrasound
– Establishes diagnosis easily
– Accurately measures infrarenal diameter
– Difficult to visualize thoracic or suprarenal
aneurysms
– Difficult to establish relationship to renal arteries
– Technician dependent
– Widely available, quick, no risk, cheap
22. Aortic Aneurysms
CT Scan
• Very reliable and reproducible
• Can image entire aorta
• Can visualize relation ship to visceral vessels
• Longer to obtain and is more costly than U/S
• Most useful
• Requires contrast agent - renal toxicity
23. Aortic Aneurysms
MRA
Now widely available
More expensive than CT
No contrast agent required
Spacial resolution less than CT
Can visualize the whole extent of the aorta in multiple planes
Ability to assess branch vessels, AI, and pericardial effusion
• In the acute setting, MRI is limited because it is less accessible, it is
• more difficult to monitor unstable patients during imaging, and it
has
• longer acquisition times than CT
Limited applicability in pts with pacemakers or metallic clips
24. TEE
TEE can image the thoracic aorta from the aortic valve to the distal
ascending aorta and from the distal aortic arch to the proximal
abdominal aorta.
The distal ascending aorta and proximal aortic arch cannot be
reliably imaged by TEE because the intervening trachea and left
mainstem bronchus obstruct the acoustic window; this is known as
the “blind spot” of TEE.
The advantages of TEE include its portability, its real-time
Interpretation, its compatibility at the bedside and in the OR, and
its multiple imaging modalities for complete aortic and cardiac
assessment.
Its disadvantages include the requirement for sedation or general
anesthesia and the risks for upper gastrointestinal injury.
25. Management strategies
Non-surgical management and surveillance
The main aim of medical therapy is to reduce shear stress on the
diseased segment of the aorta by reducing blood pressure and
cardiac contractility
The most important medical management steps are as follows:
(i) Smoking cessation can slow down aneurysmal growth by 15– 20%
and decrease perioperative morbidity relating to wound healing
and cardiorespiratory complications.
(ii) Statins can minimize perioperative myocardial ischaemia
(iii) According to recent recommendations, low-dose aspirin should
be started when an AAA is diagnosed and continued indefinitely may
alter aneurysmal growth
.
26. • Control of both blood pressure and ejection velocity
are the mainstays of hemodynamic optimization of the
patient with an aortic lesion to prevent aneurysm
rupture.
• Aggressive control of blood pressure with vasodilators
is likely to cause a reflex tachycardia and an increase in
left ventricular change in pressure over change in time
LV (dp/dt), thereby increasing ejection velocity and the
sheer forces on the aortic lesion.
• Simultaneous control of both blood pressure and
ejection velocity is best obtained with a combination of
beta-blockers and vasodilators
27. • In patients with Marfan syndrome, prophylactic use of
beta-blockers, angiotensin-converting enzyme (ACE)
inhibitor, and angiotensin II receptor blocker seem to
be able to reduce either the progression of the aortic
dilation or the occurrence of complications
• In chronic conditions, blood pressure should be
controlled below 140/90 mm Hg, with lifestyle changes
and use of antihypertensive drugs, if necessary
28. SCREENING
• Data from the United Kingdom Multicentre Abdominal
Aortic Aneurysm Screening Study (MASS) have shown that
for patients with AAA diameters greater than 55 mm
measured by ultrasonography, the number needed to treat
(NNT) with elective AAA repair to prevent one death from
AAA over the following four years
• The United Kingdom Small Aneurysm Trial showed that
patients with AAA antero-posterior diameters of 40 to 54
mm measured by ultrasonography randomized to elective
surgical treatment were more likely to die from an AAA-
related cause than those randomized to best medical
treatment and screening
33. PRE OP EVALUATION
• A preoperative history and examination reveals stridor, wheezing,
cough, or tracheal deviation should raise suspicion of aortic
impingement and possible tracheomalacia.
• Unilateral vocal cord paralysis, which results from compression of
the recurrent laryngeal nerve between the aorta and trachea, may
present clinically as voice hoarseness.
• Preoperative pulmonary function testing with flow–volume loop
analysis will reveal an intrathoracic obstructive process in severe
cases.
• Radiographic studies may be useful in delineating the extent of
airway compromise caused by aortic lesions.
34. PRE OP AIRWAY ASSESSMENT
• The trachea is markedly
deviated secondary to an
aortic aneurysm.
• The trachea and left
mainstem bronchus may
be compressed from an
aortic aneurysm.
• Left-sided double lumen
endotracheal tubes may
be difficult to place in
these patients
35. Incidence of coexisting diseases in patients with
aortic pathology presenting for surgery
• Coronary artery disease 66%
• Hypertension 42%
• Chronic obstructive pulmonary disease 23%
• Peripheral vascular disease 22%
• Cerebrovascular disease 14%
• Diabetes mellitus 8%
• Other aneurysms 4%
• Chronic renal disease 3%
36. Cardiac Assessment
• Because myocardial ischemia is an important predictor of perioperative
outcome, it has featured prominently in the guidelines for thoracic aortic
diseases.
• Patients with evidence of myocardial ischemia should undergo further
evaluation to determine the extent and severity of coronary artery disease
(CAD; ACC/AHA Class I recommendation; level of evidence C).
• If significant CAD is responsible for an acute coronary syndrome, then
coronary revascularization is indicated before or concomitant with the
thoracic aortic procedure (ACC/ AHA Class I recommendation; level of
evidence C).
• Concomitant coronary artery bypass grafting (CABG) is reasonable in
patients who have not only stable but significant CAD, but who are also
scheduled to undergo surgery for diseases of the ascending aorta or aortic
arch, or both (ACC/AHA Class IIa recommendation; level of evidence C
37. Assessment of organ systems
• 1. Neurologic. patient should be monitored closely for
change in neurologic status, as this is an indication for
immediate surgical intervention. Involvement of the artery
of Adamkewitcz may lead to lower extremity paralysis,
while propagation of a dissection into a cerebral vessel may
lead to a change in mental status or stroke symptoms.
• 2. Renal function. Urine output should be followed, as
development of anuria or oliguria in the euvolemic setting
is an indication for immediate surgical intervention.
• 3. Gastrointestinal. Serial abdominal examinations should
be performed, and blood gas analysis should be done
routinely to assess changes in acid-base status. Ischemic
bowel can cause significant metabolic acidosis
38. PRE OP MEDICINE
• According to recent recommendations, patients should continue
• taking b-blockers (if already taking these), aspirin, and statins
before surgery.
• Diuretics and ACE inhibitors should be considered on a case-by-
case basis.
• Decisions regarding continuation of clopidogrel and newer
antiplatelet agents ( prasugrel, ticagrelor) through the perioperative
period are more complex and depend on the indication for these
agents;
• Although there is an increased risk of perioperative bleeding,
recent data suggest that continuation of clopidogrel may not
increase transfusion requirements or the incidence of reoperation
for bleeding after AAA repair
39. Bleeding and transfusion
• Coagulopathy frequently encounterd
• Many pt require Lt heart or full CPB during Sx, CPB may
cause consuptive coagulopathy & enhanced
fybrinolysis, thus ↑ing bl. Loss
• DHCA may cause platelete dysfunction secondary to
extream hypothermia
• So prepare total of 8 to 10 units of PCV, FFP & PC
• Blood scavenging & reprocessing
• Antifibrinolytic therapy during aortic surgery is
controversial but commonly used eg. Trenexamic acid,
ƐACA,Aprotinin
40. Monitoring
Minimum standard monitoring should be placed before induction of
anaesthesia.
A five-lead ECG is more sensitive in detecting myocardial ischaemia.
Invasive arterial pressure monitoring should be established before but
central venous access is usually secured after induction of anaesthesia.
Urinary catheterization and temperature monitoring
Neuromonitoring
Different cardiac output monitoring strategies have their limitations and
may respond slowly to haemodynamic changes with aortic cross-clamp
application and release.
Oesophageal Doppler uses flow velocity in the aorta to calculate cardiac
output and is unreliable when the aorta is clamped.
Pulse wave contour analysis cardiac output and other monitors are gaining
popularity, but their use has not yet been fully evaluated in aortic surgery
41. ARTERIAL CANNULATION
• A right radial arterial catheter is preferred for most cases.
• If arterial cannulation of the right axillary, subclavian, or
innominate artery is planned for CPB and ACP, bilateral radial
arterial catheters often are required to measure cerebral and
systemic perfusion pressures
• Asc. Aortic lesion may involve the Innominate A., so Lt Radial or
femoral line is inserted for direct BP monitoring.
• If Rt. Axillary cannulation is used arterial pr measurement will be
falsely elevated bec. Of increased flow.
• In case of Descending aortic and thoracoabdominal aneurysms
(TAA) Arterial monitoring lines are inserted in the right radial and
femoral arteries to monitor proximal and distal pressures during the
period of aortic cross-clamping. The femoral line is valuable when
left-heart bypass techniques are used
42. Induction
Anaesthesia is no different from that for conventional open heart sx
The induction of general anesthesia requires careful hemodynamic monitoring
with anticipation of changes because of anesthetic drugs and tracheal intubation.
• Appropriate vasoactive drugs should be immediately available as required.
• Avoid hypertension to increases forward flow in AR and minimizes the risk for
aneurysm rupture.
Concomitant vasodilator infusions often are discontinued before anesthetic
induction.
Because etomidate does not attenuate sympathetic responses with no direct
effects on myocardial contractility, it may be preferred in the setting of
hemodynamic instability.
In elective cases, anesthetic induction can proceed with routine intravenous
hypnotics, followed by narcotic titration for attenuation of the hypertensive
responses to tracheal intubation and skin incision.
General anesthetic maintenance is typically with a balanced technique with
narcotic and inhalation agent , neuromuscular blockade is achieved by titration of
a nondepolarizing muscle relaxant
43. Surgical repair in different type of
aortic aneurysm
• The type of surgical repair depends on aortic valve function
and the aneurysm extent.
• The most common aortic valve diseases associated with
ascending aortic aneurysm are bicuspid aortic valve or AR
caused by dilation of the aortic root.
• If the aortic valve and aortic root are normal, a simple tube
graft can be used to replace the ascending aorta.
• If the aortic valve is diseased but the sinuses of Valsalva are
normal, an aortic valve replacement combined with a tube
graft for the ascending aorta without need for
reimplantation of the coronary arteries can be performed;
ACC/AHA class I recommendation; level of evidence C).
44. • If disease also involves the aortic valve and the aortic
root, the patient requires aortic root replacement and
aortic valve intervention.
• If technically feasible, the aortic valve can be
reimplanted with a modified David technique, which
includes graft reconstruction of the aortic root with
reimplantation of the coronary arteries (ACC/AHA Class
I recommendation; level of evidence C).
• If not feasible, aortic root replacement with a
composite valve-graft conduit is indicated (Bentall
procedure ACC/AHA Class I recommendation; level of
evidence C).
45. Surgery in aortic arch aneurysm
• For ascending aortic aneurysms that involve only the proximal aortic arch,
partial arch replacement (hemiarch technique) is reasonable in which a
tubular graft is interposed between the ascending aorta or aortic root and
the underside of the aortic arch (ACC/AHA Class IIa recommendation;
• Ascending aorta with hemiarch reconstruction often is performed using
DHCA with or without ACP/RCP to make the distal anastomosis feasible
without cross-clamping (“open technique”).
• In patients who have isolated aortic arch aneurysms and who have a low
operative risk, arch replacement is reasonable when the arch diameter
exceeds 5.5 cm (ACC/AHA Class IIa recommendation;
• Total aortic arch replacement is reasonable in aneurysms that involve the
entire arch (ACC/AHA Class IIa recommendation
• Ascending aortic aneurysms that extend through the aortic arch into the
descending aorta can be repaired with the “elephant trunk” technique
ACC/AHA Class IIa recommendation;
46. CANNULATION FOR CPB
If the aneurysm ends in the proximal or midportion of the ascending aorta, the arterial cannula for
CPB can be placed in the upper ascending aorta or proximal arch.
Femoral artery cannulation is particularly useful in emergency situations with hemodynamically
unstable pa tients. However, it creates retrograde flow in the abdominal and thoracic aorta, it is a
potential cause of embolic stroke in patients with heavy atherosclerotic burden
Most recommeded and newer approach is to cannulate the right axillary , or occasionally the right
carotid, artery, allowing perfusion into the innominate artery and then into the aorta in an
antegrade manner
Most commonly venous drainage by right atrial dual-stage cannula, bicaval cannulae, .
Femoral venous cannulation is routinely used in hemodynamically unstable patients who require
pump support before sternotomy and is particularly useful in patients who are at risk of aortic
injury during sternotomy. In patients undergoing reoperation and large ascending aortic aneurysms
abutting the sternum
47. • During systemic cooling in aortic aneurysm surgery the heart will spontaneously
fibrillate. At this time, a left ventricular VENT is inserted through the right superior
pulmonary vein to decompress the left ventricle. This is especially important in
patients who are prone to ventricular distention, such as those with aortic valve
regurgitation.
• To prevent this complication, the Vent is generally placed before systemic cooling
begins.
• If the patient has an incompetent aortic valve, as may be the case in an aortic
dissection, manual compression of the distending heart may be necessary at this
time
• Other advantage of LV vent are to
Minimizes preload,
Prevents ventricular distention,
Reduces myocardial rewarming,
Prevents ejection of air,
Facilitates exposure of the aortic valve.
48. MYOCARDIAL PROTECTION
• Cardioplegia is achieved with the use of a cold hyperkalemic
crystalloid or blood cardioplegic solution, which may be administered
in one of several ways:
(a) antegrade aortic root administration if the aorta can be cross-
clamped and the aortic valve is competent,
(b) direct coronary ostial administration after opening of the
ascending aorta, or
(c) retrograde administration through the coronary sinus.
• When the aortic arch is included in the procedure and when cross-
clamping of the ascending aorta is not possible because of excessive
friability of the aortic tissues, DHCA is required.
49. TEE
• Perioperative TEE can evaluate the aortic valve
structure and function to guide and assess the surgical
intervention (reimplantation,repair, replacement).
• Furthermore, TEE can assess the diameters of the
aortic root, ascending aorta, and aortic arch to guide
intervention..
• In patients with AR, TEE can assist in the conduct of
CPB by guiding placement of cannulae such as the
retrograde cardioplegia cannula (coronary sinus) and
by monitoring left ventricular (LV) volume to ensure
that the LV drainage cannula keeps the ventricle
collapsed.
51. DEEP HYPOTHERMIA AND
CIRCULATORY ARREST
• Deep hypothermia is the mainstay of any operation that
requires opening the distal ascending aorta or transverse
aortic arch where blood flow to the brain must be
interrupted.
• Although there may be controversy about the best
method of cerebral perfusion during surgeries that
involve the aortic arch, deep hypothermia alone will
usually provide the surgeon with a safe arrest period of
30 minutes, provided the patient's brain is cooled to
<20°C.
52. Conduct of DHCA
• The cooling phase should be gradual and long enough(20-30 mins) to
achieve homogenous allocation of blood to various organs and to prevent
a gradual updrift of temperature during DHCA
• The most effective method of cooling for DHCA is core cooling on high-
flow CPB.
• Cooling temperatures never exceeding 10° C differences between the
perfusate temperature (circuit) and the patient core temperature.
• Perfusate temperature is maintained between 10° C and 15° C during
cooling.
• A vasodilator such as sodium nitroprusside or phentolamine (0.2 mg/kg)
may be administered into the CPB circuit as core cooling commences to
promote vasodilation and more homogenous cooling
53. Organ protection during DHCA
• Hypothermia
• Pharmacological adjuncts
• Perfusion strategies
• Topical external cooling of the head
• optimized acid-base management
• pump prime modifications
• leukocyte depletion
• The degree of hemodilution
• strategies of cooling and rewarming
54. α-stat vs pH-stat
• pH-stat strategy results in greater cerebral blood flow, greater
efficiency, and uniformity of brain cooling, and higher brain
oxyhemoblobin saturation and less reduced cytochrome a,a3
signifying more oxygen at the mitochondrial level than α-stat blood
gas management
• However, other data suggest that cerebral metabolic recovery after
DHCA may be better with the α-stat method than with the pH-stat
mode
• Some institute use crossover strategy in which a pH-stat approach is
used during the first 10 minutes of cooling to provide maximal
cerebral metabolic suppression, followed by an α-stat strategy to
remove the severe acidosis that accumulates during profound
hypothermia during pH-stat
55. Rewarming strategies
There is no more than 10° C temperature differential
between the core and perfusate temperatures.
Patients should warm at the same rate at which they
were cooled.
Warming rate should never exceed 1° C core
temperature increase per 3 minutes of bypass time.
Use of vasodilators to facilitate distal perfusion
Treat metabolic acidosis agressive
Termination of warming should occur when the
nasopharyngeal temperature is between 35° C and 36°
C. This mild hypothermia provides additional cerebral
protection in the early postoperative period.
56. Pharmacologic Neuroprotection
There are no proven pharmacologic regimens that have demonstrated
effectiveness for decreasing the risk or severity of neurologic injury in the
setting of thoracic aortic operations.
The agents that have been reported in aortic arch series include
thiopental, propofol, steroids, magnesium sulfate, and lidocaine
Furthermore, there is considerable variation in practice with these agents
in aortic arch repair
The technique of DHCA with pharmacologic adjuncts is a reasonable
approach for neuroprotection during aortic arch surgery in the setting of
an institutional protocol and adequate institutional experience (ACC/AHA
Class IIa recommendation; level
57. Retrograde cerebral perfusion
• RCP is performed by infusing cold oxygenated blood
into the superior vena cava cannula at a temperature
of 8° C to 14° C via CPB
• The internal jugular venous pressure is maintained at
less than 25 mm Hg to prevent cerebral edema
• Patient is positioned in 10 degrees of Trendelenburg
to Decrease the risk for cerebral air embolism and
prevent trapping of air
• Flow rates of 200 to 600 mL/min usually can be
achieved
58. • Advantage are more homogeneous cerebral cooling;
washout of air bubbles, embolic debris, and metabolic
waste products; prevention of cerebral blood cell
microaggregation; and delivery of oxygen and
nutritional substrates to brain tissue
• During RCP, only a minimal amount of blood (not more
than 3% to 10%) is directed to the brain, whereas more
than 90% is deviated through the azygos to the SVC or
entrapped in the cerebral venous sinuses
59. Anterograde cerebral perfusion
• Arterial CPB circuit flow can be delivered selectively to the
cerebral circulation antegrade via the circle of Willis following
cannulation of the innominate artery or right carotid artery
• ACP may be unilateral or bilateral, there remains controversy about
which ACP technique is superior. A recent literature Showed the
period of safe ACP was significantly prolonged with bilateral ACP
compared with unilateral ACP (30–50 minutes). The evidence favors
bilateral ACP in the setting of aortic arch repair times longer than 60
minutes
• The technique of DHCA with ACP is a reasonable approach for
neuroprotection during aortic arch surgery in the setting of
adequate institutional experience (ACC/AHA Class IIa
recommendation; level of evidence B).
60. GOALS OF Anaesthetic management
IN TAAA OPEN REPAIR
• Anaesthetic management focuses on the
Acute haemodynamic changes with aortic
cross-clamping and unclamping,
Maintaining organ perfusion and oxygenation
Attenuating ischaemic reperfusion injury,
Providing intra- and postoperative analgesia
61. Lung Isolation Techniques
• Selective ventilation of the right lung with
concomitant left lung Collapse during TAAA repair
enhances surgical access and protects the right
lung from left lung bleeding.
• Collapse of the left lung typically is achieved
when the left main bronchus is intubated either
with a double-lumen endobronchial tube (DLT) or
a bronchial blocker.
• The advantages of a left DLT include the ability to
apply selective continuous positive airway
pressure to the left lung
62. analgesia
A thoracic epidural catheter is usually placed before
induction of anaesthesia at a level corresponding to
the upper dermatomal level of the incision (usually T8–
T10) for Postoperative analgesia
Intraoperative analgesia can be provided using opioids
or by using epidural analgesia;
however, high doses of epidural local anaesthetics can
cause profound hypotension after aortic crossclamp
release due to sympathetic blockade.
It is common practice to limit epidural local
anaesthetic administration until after crossclamp
release and haemostastis has been achieved.
63. Heparin 75–150 units kg21 is given i.v. before aortic
crossclamp application.
Activated clotting time can be used to guide heparin
therapy (2–3 times more than baseline).
Cell salvage equipment should be used when available.
Serial arterial blood gas samples are usually analysed
to monitor respiratory and metabolic status.
Facilities for the rapid infusion of warm fluids and
blood should be available for immediate use.
All efforts should be made to maintain normothermia;
however, lower body warming during aortic cross-
clamp application is discouraged
64. RECOMMENDATION FOR PERFUSION
TECHNIQUE
Descending thoracic aortic repairs
Left heart bypass for high-risk patients (acute dissection, rupture,
prior abdominal aortic aneurysm repair)
Extent I and II thoracoabdominal repairs
Left heart bypass during proximal anastomosis
Selective perfusion of celiac axis and superior mesenteric artery
during intercostal and visceral anastomoses
Perfusion of renal arteries with 4°C crystalloid solution
Extent III and IV thoracoabdominal repairs
Perfusion of renal arteries with 4°C crystalloid solution
65. Open repair of TAAA typically is accomplished
by one of three major PERFUSION techniques;
(1) aortic cross-clamping,
(2) aortic cross- clamping with a Gott shunt,
(3) aortic cross-clamping with PLHB or partial
CPB
66. Simple Aortic Cross-Clamp Technique
• Its major Disadvantage is the concomitant vital organ
ischemia below the aortic clamp.
• Its further disadvantages include proximal aortic
hypertension, Bleeding, and hemodynamic instability
on reperfusion.
• Proximal aortic hypertension may induce LV Ischemia.
• Mild systemic hypothermia and selective spinal cooling
protect against the ischemia associated with this
technique.
• Despite its physiologic consequences, this technique
remains popular because it is simple and has proven
clinical outcomes
67. Gott Shunt
The Gott shunt allows passive
shunting of blood from the proximal
to distal aorta during aortic cross-
clamping for thoracic aortic repair
Blood flow from the proximal to
distal aorta through the Gott shunt
depends on proximal aortic
pressure, shunt length and diameter,
and distal aortic pressure.
Monitoring the femoral arterial
pressure facilitates assessment of
distal aortic perfusion and shunt
flow.
The advantages of the Gott shunt
are its simplicity, its low cost, and its
requirement for only partial
anticoagulation.
68. Partial Left-Heart Bypass
• The control of both proximal and
distal aortic perfusion during TAAA
repair is achieved with PLHB.
• This technique requires left atrial
cannulation, usually via a left
pulmonary vein
• Oxygenated blood from the left
atrium flows through the CPB circuit
into the distal aorta or a major
branch via the arterial Cannula.
• The degree of heparinization for
PLHB is minimal with heparin-coated
circuits without an oxygenator.
• Full systemic anticoagulation with
ACT greater than 400 seconds is
required for CPB circuits with
membrane oxygenators and heat
exchangers
69. • During PLHB, the proximal mean arterial pressure (MAP; radial artery) is
generally maintained in the 80 to 90 mm Hg range.
• Flow rates in the range of 1.5 to 2.5 L/min typically maintain a distal aortic
MAP in the 60 to 70 mm Hg range, monitored via a femoral arterial
catheter.
• Sequential advancement of the aortic crossclamp during PLHB permits
segmental aortic reconstruction with a decrease in end-organ ischemia.
• The advantages of PLHB include control of aortic pressures and systemic
temperature, reliable distal aortic perfusion, and selective antegrade
perfusion of important branch vessels
70. Advantages of distal perfusion
• Control of proximal hypertension
• Decrease left ventricular afterload
• Less hemodynamic perturbations with aortic clamping and
unclamping
• Decrease duration of mesenteric ischemia
• Decrease risk for paraplegia from spinal cord ischemia
• Ability to control systemic temperature with heat exchanger
• Vascular access for rapid volume expansion
• Ability to oxygenate blood with extracorporeal oxygenator
• Capability to selectively perfuse mesenteric organs or aortic branch
vessels
• Maintain lower extremity SSEPs and MEPs for neurophysiologic
monitoring
71. aortic cross-clamping
The physiological effect of aortic cross-clamping during
surgery varies with the level of the clamp in relation to
the main aortic branches.
Perfusion to the lower half of the body is therefore
dependent on collateral circulation while the clamp is
applied.
Clamp application increases the afterload of the heart
and a sudden increase in arterial pressure proximal to
the clamp; this can be ttenuated with vasodilators [e.g.
glyceryl trinitrate (GTN), sodium nitroprusside],
opioids, or deepening of anaesthesia.
72. • Increased afterload and left ventricular end-
diastolic volume both increase myocardial
contractility and oxygen demand.
• This increase in myocardial oxygen demand is
usually met by an increase in coronary blood flow
and oxygen supply, but can cause myocardial
ischaemia
• The mean arterial pressure should be maintained
within the autoregulation limits of vital organs.
73. aortic cross-clamp release
After aortic cross-clamp release, peripheral vascular resistance
decreases by 70–80%, causing a decrease in arterial pressure.
Hypotension can also be caused by blood sequestration in the
lower half of the body, ischaemia–reperfusion injury, and the
washout of anaerobic metabolites causing metabolic (lactic) acidosis.
This can cause direct myocardial suppression and profound
peripheral vasodilatation. Coronary blood flow and left ventricular
end-diastolic volume also decrease (almost 50% from pre-clamp
levels) after clamp release
74. MANAGEMENT OF AORTIC
CROSSCLAMP RELEASE
• Strategies to manage hypotension after aortic cross-clamp release include
Discontinue vasodilator agents
Gradual release of the clamp,
Volume loading,
Vasoconstrictors, or
Positive inotropic drugs (e.g. ephedrine, termine phenylephrine,
epinephrine, and norepinephrine).
• It is important to be aware that vasoactive drugs should only be used after
adequate volume repletion
• TEE can adequately assist with LV volume assessment.
• Acidosis may be treated with hyperventilation and bolus administration of
sodium bicarbonate.
• A continuous infusion of bicarbonate (0.05 mEq/kg/min) during cross-
clamping may be more efficacious.
75. RENAL PROTECTION
• The main cause of renal complications after AAA repair is the
decrease in renal blood flow, decreased renal perfusion pressure
(outside autoregulation) augmented by the increasing renal
vascular resistance (by 30%) associated with aortic clamping.
• Myoglobin release from ischaemic tissues may contribute to acute
tubular necrosis by decreasing local nitric oxide release.
• Acute kidney injury (AKI) may also be linked to ischaemic– perfusion
injury, decreased renal cortical blood flow, prostaglandin imbalance,
and increased activity of renin–angiotensin system.
• Postoperative dialysis rates are similar in patients who have
undergone either suprarenal or infra-renal aortic cross-clamping
76. • Rhabdomyolysis from lower extremity ischemia was recently
identified as a mechanism for renal dysfunction after TAAA repair.
• The maintenance of lower extremity perfusion bilaterally during
distal aortic perfusion has been shown to ameliorate this
rhabdomyolysis with a significant nephroprotective effect
• intraoperative cold renal perfusion with blood or crystalloid is
recommended as a reasonable intraoperative nephroprotective
strategy during TAAA repair (ACC/AHA Class IIb recommendation;
level of evidence C).
77. • The thoracic aortic guidelines recommend preoperative
hydration and intraoperative mannitol administration as
reasonable nephroprotective strategies in extensive distal
open thoracic aortic repairs, including TAAA repair
(ACC/AHA Class Iib recommendation; level of evidence C).
• Several drugs (dopamine, N-acetyl cysteine, mannitol,
furosemide) have been used in an attempt to protect
against AKI, although none has been shown consistently to
be beneficial, and all diuretics should be used only after
adequate fluid replacement and volume loading.
• Mannitol can increase renal blood flow during aortic cross-
clamp; however, both mannitol and dopamine use fail to
return GFR to baseline levels after operation
78. PARAPLEGIA IN TAAA REPAIR
• Paraplegia after TAAA repair is a
devastating complication.
• most patients, one radicular arterial
branch, known as the great radicular
artery (of Adamkiewicz), provides a
major portion of the blood supply to
the midportion of the spinal cord. It
may arise anywhere from T5 to below
L1
• The temporary interruption of distal
aortic perfusion and sacrifice of
spinal segmental arteries during
TAAA repair are central events in the
pathogenesis of spinal cord ischemia
and paraplegia
•
79. Factors That Contribute to Paraplegia after Thoracic
or Thoracoabdominal Aneurysm repair
Duration of aortic cross-clamp
Thoracoabdominal aortic
aneurysm extent
Hypotension or cardiogenic shock
Emergency surgery
Aortic rupture
Presence of aortic dissection
Sacrifice of intercostal or
segmental artery branches
Prior thoracic or abdominal aortic
aneurysm repair
Occlusive peripheral vascular
disease
Anemia
80. Techniques to Decrease the Risk
for Intraoperative Spinal Cord Ischemia
Distal aortic perfusion
Arterial pressure augmentation
Minimizing the ischemic time
Mild systemic hypothermia
Lumbar cerebrospinal fluid drainage
Selective spinal cord cooling
Segmental aortic reconstruction
Intercostal artery preservation
Pharmacologic neuroprotection
Intraoperative motor- or somatosensory-evoked potential
monitoring
81. Minimize Aortic Cross-clamp Time
Distal aortic perfusion
• Passive shunt (Gott)
• Partial left heart bypass
• Partial cardiopulmonary bypass
Deliberate Hypothermia
• Mild-to-moderate systemic hypothermia (32° C to 35°
C)
• Deep hypothermic circulatory arrest (14° C to 18° C)
• Selective spinal cord hypothermia (epidural cooling,
25˚ C)
82. Increase Spinal Cord Perfusion
Pressure
• Reimplantation of critical intercostal and
segmental arterial branches
• Lumbar cerebrospinal fluid (CSF) drainage (CSF
pressure ≤ 10 mm Hg)
• Arterial pressure augmentation (mean arterial
pressure ≥ 85 mm Hg)
83. spinal drain management
• SCPP is estimated as the MAP minus the lumbar CSF
pressure.
• In general, the SCPP should be maintained greater than 70
mm Hg
• 30% or more of all neurologic deficits are delayed in onset
• spinal drains are commonly left in for 48 hours
postoperatively and are replaced if neurologic deficits occur
after the drain is removed.
• maintain CSFP between 10 to 15 mm Hg in the
postoperative setting, efforts must be made to avoid
systemic hypotension and associated decreased spinal cord
perfusion.
•
84. Intraoperative Neurophysiologic
Monitoring
• Neurophysiologic monitoring of the spinal cord (SSEPs
and/or MEPs) is recommended as a strategy for the
diagnosis of spinal cord ischemia so as to allow immediate
intraoperative neuroprotective interventions such as
intercostal artery implantation, relative arterial
hypertension, and CSF drainage (ACC/AHA Class IIb
recommendation; level of evidence B).
• Because SSEP monitors posterior spinal column integrity,
MEPs have been advocated because they monitor the
anterior spinal columns that are most common at risk
during TAAA repair.
85. Spinal Cord Hypothermia
Although DHCA is effective, moderate systemic hypothermia is also
reasonable for spinal cord protection during TAAA repair (ACC/AHA
Class IIa recommendation; level of evidence B).
Furthermore, topical spinal cord hypothermia is possible with cold
saline epidural infusion to avoid ischemia during TAAA repair.
Epidural cooling is recommended as an adjunctive technique for
spinal cord protection during major distal thoracic aortic
reconstructions (ACC/AHA Class IIb recommendation; level of
evidence B).
This technique give adjunctive benefit and the recent clinical
development of a specialized countercurrent closed-lumen epidural
catheter for epidural cooling during major distal aortic
reconstructions
86. Pharmacologic Protection of the Spinal
Cord
• Pharmacologic spinal cord protection with agents
such as high dose systemic glucocorticoids,
mannitol, intrathecal papaverine, and anesthetic
agents is recommended as an adjunctive
technique in a multimodal neuroprotective
protocol (ACC/AHA Class IIb recommendation;
level of evidence B).
• Additional neuroprotective agents that have
been studied in this regard include lidocaine,
naloxone, and magnesium
87. TEVAR
• Thoracic endovascular aortic repair aims at
excluding an aortic lesion (i.e. aneurysm or FL
after AD) from the circulation by the
Implantationof a membrane-covered stent-
graft across the lesion, in order to prevent
further enlargement and ultimate aortic
rupture
89. TEVAR Anesthetic Protocol
• Always GA for TEVAR
• For EVAR General Anesthesia ,Regional Anesthesia
(epidural alone or spinal or combined) or Local Anesth
(local groin infiltration) with sedation
• Assess risk of SCI
• Consider spinal drain
• Neuromonitoring
• Arterial line The right radial artery is preferred for
• blood pressure monitoring, given that the left subclav
artery frequently may be covered and/or the left brac
artery may be accessed as part of the procedure.
• PAC monitoring may be helpful in the setting of signif
90. GA VS REGIONAL OR LOCAL
• Risk‐adapted Outcome after Endovascular Aortic
Aneurysm Repair: Analysis of Anesthesia Types Based
on EUROSTAR data
• Ruppert et al. Journal of Endovascular Therapy, 2007.
• between 1997 and 2004, 164 centers, 5557 patients
• Patients were divided into low‐risk (ASA I or II.), high
risk(ASA III or IV), LA, GA, RA into 6 groups.
• Low‐risk group: 78.8% GA, 15.9% had RA, 5.3% LA
• High‐risk group: 60.4 % GA, 33.7% RA, 5.9% LA
91. • Outcomes
• • GA vs. RA or LA:
• less systemic complications
(cardiac, cerebral,
pulmonary, renal,
• hepatobiliary, sepsis)
• • GA versus RA: less 30 days
early death in the RA group
• • Less ICU admission with
local and regional (low risk
and high risk )
92. • Observation from the IMPROVE trial (BJS 2014)
• Prospective multicenter, observational study on
Anesthesia type in 558 patients with a
symptomatic or ruptured aneurysm ( EVAR )
• Lowest blood pressure (<70 MAP) was strongly
and independently associated with 30‐days
mortality
• • EVAR with local anesthesia (adjusted to
variables) alone had greatly reduced (4 fold) 30
days mortality
93. pre-procedural planning
• Contrast-enhanced CT
represents the imaging
modality of choice for
planning TEVAR, taking ,3
mm ‘slices’ of the proximal
supra-aortic branches down
to the femoral arteries
RECOMMENDATION FOR TEVAR
94. TEE IN TEVAR
• Intraoperative TEE is reasonable in thoracic
aortic procedures, including endovascular
interventions, in which it assists in
hemodynamic monitoring, procedural
guidance, and endoleak detection (ACC/AHA
Class IIa recommendation; level of evidence
95. Complications
• Immediate conversion to open surgery is required in
approximately 0.6% of patients.
• .
• The rates of vascular injury after EVAR are low
(approximately 0–3%), due to careful pre-procedural
planning.
• The incidence of stent-graft infection after EVAR is ,1%,
with high mortality.
• Graft migration
• Embolisation
96. Classification of
endoleaks.
Endoleak is the most
common complication of
EVAR.
Type I and Type III
endoleaks demand
correction (proximal cuff
or extension),
Type II endoleak may
seal spontaneously in
about 50% of cases
97. spinal cord
ischemia after TEVAR or EVAR
• perioperative hypotension (decreased SCPP),
• prior abdominal/descending thoracic aortic
procedures (compromised spinal collateral
arterial network)
• coverage of the entire descending thoracic
aorta (significant loss of intercostal arteries
98. Spinal cord protection protocol
• Place CSF drain the pre procedure
• Record opening pressure, zero at RA level
• If pressure exceeds 12 mmHg, pressure goal < 10mmHg
• Limit CSF drain to less than 20 ml over 1st‐hr
• Limit CSF drain to less than 40 ml over 4‐hours
• If SSEP signal decrease drain 10 ml
• MAP > 90 hgmm post‐TEVAR
• Clamp drain after confirming bilateral lower extremity
function
• Remove drain after 24 hrs of clamping
• Reopen/Drain if delayed paraparesis/paraplegia
• If CSF turns bloody turn off drain
Type I: Leak at graft attachment site above, below, or between graft components (Ia: proximal attachment site; Ib: distal attachment site).
Type II: Aneurysm sac filling retrogradely via single (IIa) or multiple branch vessels (IIb).
Type III: Leak through mechanical defect in graft, mechanical failure of the stent-graft by junctional separation of the modular components (IIIa), or
fractures or holes in the endograft (IIIb).
Type IV: Leak through graft fabric as a result of graft porosity.
Type V: Continued expansion of aneurysm sac without demonstrable leak on imaging (endotension, controversial