Atrial Fibrillation
Echocardiography, Doppler
Echocardiography, Doppler, Pulsed
Pericardiectomy
Electric Countershock
Ventricular Function, Left
Echocardiography
Echocardiography, Transesophageal
Stroke Volume
Observer Variation
Blood Flow Velocity
Hemodynamics
Ventricular Dysfunction, Left
Effects of pacing-induced and balloon coronary occlusion ischemia on left atrial function in patients with coronary artery disease. (1/343)
OBJECTIVES: The aim of this study was to compare left atrial (LA) function in 16 patients with distal left anterior descending (LAD) and in 16 patients with proximal left circumflex (LCx) coronary artery stenosis at rest and immediately after pacing-induced tachycardia (LAD-pacing [P] and LCx-P) or coronary occlusion (LAD-CO and LCx-CO). BACKGROUND: During left ventricular (LV) ischemia, compensatory augmentation of LA contraction enhances LV filling and performance. The left atrium is supplied predominantly by branches arising from the LCx. Therefore, we hypothesized that one mechanism for the loss of atrial contraction may be ischemic LA dysfunction. METHODS: Left ventricular and LA pressure-area relations were derived from simultaneous double-tip micromanometer pressure recordings and automatic boundary detection echocardiograms. RESULTS: Immediately after pacing or after coronary occlusion, LV end-diastolic pressure, LV relaxation, LA mean pressure and LV stiffness significantly increased in all patients. However, the area of the A loop of the LA pressure-area relation, representing the LA pump function, significantly decreased in groups LCx-P and LCx-CO (from 14+/-3 to 9+/-2, and from 16+/-4 to 9+/-2 mm Hg.cm2, respectively, p < 0.05), whereas it increased in groups LAD-P and LAD-CO (from 12+/-3 to 54+/-10, and from 16+/-3 to 49+/-8 mm Hg.cm2, respectively, p < 0.001). CONCLUSIONS: In patients with LAD stenosis, LV supply or demand ischemia is associated with enhanced LA pump function. However, in patients with proximal LCx stenosis who develop the same type and degree of ischemia, LA branches might have been affected, rendering the LA ischemic and unable to increase its booster pump function. (+info)Pulmonary venous flow in hypertrophic cardiomyopathy as assessed by the transoesophageal approach. The additive value of pulmonary venous flow and left atrial size variables in estimating the mitral inflow pattern in hypertrophic cardiomyopathy. (2/343)
AIMS: This study was conducted to assess the characteristics of the pattern of pulmonary venous flow and to document the interaction of this flow and left atrial function with the pattern of mitral inflow in hypertrophic cardiomyopathy. METHODS AND RESULTS: Pulmonary venous and mitral flows were evaluated by the transoesophageal approach in 80 patients with hypertrophic cardiomyopathy. Left atrial size and function were measured by the transthoracic approach. Their values were compared with those obtained from 35 normal controls. Twelve patients showed significant (> 2+) mitral regurgitation. As a group, hypertrophic cardiomyopathy patients showed increased atrial reversal flow and longer deceleration time of the diastolic wave, but a wide variability of pulmonary venous flow patterns were observed. Thirty patients (37.5%) had pseudonormal mitral flow patterns. Stepwise multilinear regression analysis identified the ratio of systolic to diastolic pulmonary venous flow velocity, the ratio of velocity-time integrals of both flow waves at atrial contraction, the left atrial minimal volume and the systolic fraction as independent predictive variables of the mitral E/A wave velocity ratio (r = 0.82). By logistic regression, the former three variables were selected as independent predictive covariates of a pseudonormal mitral flow pattern (sensitivity: 83%, specificity: 90%). The ratio of velocity-time integrals of both atrial waves was the most important predictive variable in both analyses. CONCLUSIONS: The observed variability in the configuration of pulmonary venous flow velocity waveform is related to what occurs in transmitral flow in patients with hypertrophic cardiomyopathy. Significant mitral regurgitation is not an independent correlate of pseudonormal mitral inflow patterns in these patients. Our results further emphasize the complementary, additive value of the pulmonary venous flow velocity pattern and left atrial size in the interpretation of the mitral flow velocity pattern, and indirectly suggest the underlying increased left ventricular filling pressures of patients with hypertrophic cardiomyopathy and pseudonormal mitral flow patterns. (+info)Doppler sonographic evaluation of left atrial function after cardioversion of atrial fibrillation. (3/343)
Restoration of sinus rhythm is not always followed by immediate return of effective atrial contraction. Left atrial mechanical function can be assessed by Doppler echocardiography; in the present study we measured the atrial ejection force, which is a noninvasive Doppler-derived parameter that measures the strength of atrial contraction. The aim of the present study was to evaluate the influence of clinical and echocardiographic parameters: duration and cause of atrial fibrillation, different modality of cardioversion, and left atrial size with respect to the delay in the return of effective atrial contraction after cardioversion. Seventy patients were randomly chosen to undergo cardioversion by either direct current shock or intravenously administered procainamide hydrochloride. The 52 patients who had sinus rhythm restored underwent a complete Doppler echocardiographic examination 1 h after the restoration of sinus rhythm and after 1 day, 7 days, and 1 month. The relation between clinical variables and atrial ejection force was tested. Atrial ejection force was greater immediately and 24 h after cardioversion in patients who underwent pharmacologic therapy compared to patients treated with direct current shock (11.3+/-3 versus 5+/-2.9 dynes; P<0.001). In both groups atrial ejection force increased over time. The mode of cardioversion was significantly associated with recovery of left atrial mechanical function by day 1 in univariate and multivariate analysis (odds ratio, 0.14; 95% confidence interval, 0.02-1.2). The other variable associated with the delay in the recovery of atrial function was a dilated left atrium (odds ratio, 0.16; 95% confidence interval, 0.12-1.6). Atrial ejection force is a noninvasive parameter that can be easily measured after cardioversion and gives accurate information about the recovery of left atrial mechanical function. The recovery of left atrial function was influenced by the mode of cardioversion and left atrial size. (+info)Importance of left atrial appendage flow as a predictor of thromboembolic events in patients with atrial fibrillation. (4/343)
AIM: The purpose of this study was to investigate the role of transoesophageal echocardiography in predicting subsequent thromboembolic events in patients with atrial fibrillation. METHODS AND PATIENTS: Transoesophageal echocardiography was performed in 88 patients with documented paroxysmal (n=53) or chronic atrial fibrillation (n=35) to assess morphological and functional predictors of thromboembolic events. Prospective selection was from patients with non-valvular atrial fibrillation who had undergone transoesophageal echocardiography because of previous thromboembolism (n=30); prior to electrical cardioversion (n=31); or for other reasons (n=27). All patients were followed up for 1 year. RESULTS: During the period of follow-up new thromboembolic events occurred in 18 of 88 patients (20%/year); 16 of these patients had a stroke and two a peripheral embolism. Univariate analysis revealed that previous thromboembolism (P<0.005; odds ratio 5.3 [CI 1.9, 12. 1]), history of hypertension (P<0.01; odds ratio 4.0 [CI 1.4, 10.4), presence of left atrial spontaneous echo contrast (P<0.025; odds ratio 3.5 [CI 1.2, 10.0]), and presence of left atrial appendage peak velocity +info)Short-term effect of atrial fibrillation on atrial contractile function in humans. (5/343)
BACKGROUND: Conversion of chronic atrial fibrillation (AF) is associated with atrial stunning, but the short-term effect of a brief episode of AF on left atrial appendage (LAA) emptying velocity is unknown. The purpose of this study was to determine whether a short episode of AF affects left atrial function and whether verapamil modifies this effect. METHODS AND RESULTS: The subjects of this study were 19 patients without structural heart disease undergoing an electrophysiology procedure. In 13 patients, LAA emptying velocity was measured by transesophageal echocardiography in the setting of pharmacological autonomic blockade before, during, and after a short episode of AF. During sinus rhythm, the baseline LAA emptying velocity was measured 5 times and averaged. AF was then induced by rapid right atrial pacing. After either spontaneous or electrical conversion, LAA emptying velocity was measured immediately on resumption of sinus rhythm and every minute thereafter. The mean duration of AF was 15.3+/-3.8 minutes. The mean baseline emptying velocity was 70+/-20 cm/s. The first post-AF emptying velocity was 63+/-20 cm/s (P=0.02 versus baseline emptying velocity). The post-AF emptying velocity returned to the baseline emptying velocity value after 3.0 minutes. The mean percent reduction in post-AF emptying velocity was 9.7+/-21% (range, 15% increase to 56% decrease). A second group of 6 patients were pretreated with verapamil (0.1-mg/kg IV bolus followed by an infusion of 0.005 mg. kg-1. min-1). In these patients, the first post-AF emptying velocity, 58+/-14 cm/s, was not significantly different from the pre-AF emptying velocity, 60+/-13 cm/s (P=0.08). CONCLUSIONS: In humans, several minutes of AF may be sufficient to induce atrial contractile dysfunction after cardioversion. When atrial contractile dysfunction occurs, there is recovery of AF within several minutes. AF-induced contractile dysfunction is attenuated by verapamil and may be at least partially mediated by cellular calcium overload. (+info)Left atrial relaxation and left ventricular systolic function determine left atrial reservoir function. (6/343)
BACKGROUND: Determinants of left atrial (LA) reservoir function and its influence on left ventricular (LV) function have not been quantified. METHODS AND RESULTS: In an open-pericardium, paced (70 and 90 bpm) pig model of LV regional ischemia (left anterior descending coronary constriction), with high-fidelity LV, LA, and RV pressure recordings, we obtained the LA area with 2D automated border detection echocardiography, LA pressure-area loops, and Doppler transmitral flow. We calculated LV tau, LA relaxation (a-x pressure difference divided by time, normalized by a pressure), and stiffness (slope between x and v pressure points of v loop). Determinants of total LA reservoir (maximum-minimum area, cm(2)) were identified by multiple regression analysis. Different mean rates of LA area increase identified 2 consecutive (early rapid and late slow) reservoir phases. During ischemia, LV long-axis shortening (LAS, LV base systolic descent) and LA reservoir area change decreased (7.3+/-0.3 [SEM] versus 5.6+/-0.3 cm(2), P<0.001) and LA stiffness increased (1.6+/-0.3 versus 3.1+/-0.3 mm Hg/cm(2), P=0.009). Early reservoir area change depended on LA mean ejection rate (LA area at ECG P wave minus minimum area divided by time; multiple regression coefficient=0.9; P<0.001) and relaxation (coefficient=4.9 cm(2)xms/s; P<0.001). Late reservoir area change depended on LAS (coefficient=8 cm/s; P<0.001). Total reservoir filling depended on LA stiffness (coefficient=-0.31 cm(4)/mm Hg; P=0. 001) and cardiac output (coefficient=0.001 cm(2)xmin/L; P=0.002). The strongest predictor of cardiac output was LA reservoir filling (coefficient=301 L/minxcm(2); P<0.001). The v loop area was determined by cardiac output, LV ejection time, tau, and early transmitral flow. CONCLUSIONS: Two (early and late) reservoir phases are determined by LA contraction and relaxation and LV base descent. Acute LV regional ischemia increases LA stiffness and impairs LA reservoir function by reducing LV base descent. (+info)Noninvasive assessment of left atrial maximum dP/dt by a combination of transmitral and pulmonary venous flow. (7/343)
OBJECTIVES: The study assessed whether hemodynamic parameters of left atrial (LA) systolic function could be estimated noninvasively using Doppler echocardiography. BACKGROUND: Left atrial systolic function is an important aspect of cardiac function. Doppler echocardiography can measure changes in LA volume, but has not been shown to relate to hemodynamic parameters such as the maximal value of the first derivative of the pressure (LA dP/dt(max)). METHODS: Eighteen patients in sinus rhythm were studied immediately before and after open heart surgery using simultaneous LA pressure measurements and intraoperative transesophageal echocardiography. Left atrial pressure was measured with a micromanometer catheter, and LA dP/dt(max) during atrial contraction was obtained. Transmitral and pulmonary venous flow were recorded by pulsed Doppler echocardiography. Peak velocity, and mean acceleration and deceleration, and the time-velocity integral of each flow during atrial contraction was measured. The initial eight patients served as the study group to derive a multilinear regression equation to estimate LA dP/dt(max) from Doppler parameters, and the latter 10 patients served as the test group to validate the equation. A previously validated numeric model was used to confirm these results. RESULTS: In the study group, LA dP/dt(max) showed a linear relation with LA pressure before atrial contraction (r = 0.80, p < 0.005), confirming the presence of the Frank-Starling mechanism in the LA. Among transmitral flow parameters, mean acceleration showed the strongest correlation with LA dP/dt(max) (r = 0.78, p < 0.001). Among pulmonary venous flow parameters, no single parameter was sufficient to estimate LA dP/dt(max) with an r2 > 0.30. By stepwise and multiple linear regression analysis, LA dP/dt(max) was best described as follows: LA dP/dt(max) = 0.1 M-AC +/- 1.8 P-V - 4.1; r = 0.88, p < 0.0001, where M-AC is the mean acceleration of transmitral flow and P-V is the peak velocity of pulmonary venous flow during atrial contraction. This equation was tested in the latter 10 patients of the test group. Predicted and measured LA dP/dt(max) correlated well (r = 0.90, p < 0.0001). Numerical simulation verified that this relationship held across a wide range of atrial elastance, ventricular relaxation and systolic function, with LA dP/dt(max) predicted by the above equation with r = 0.94. CONCLUSIONS: A combination of transmitral and pulmonary venous flow parameters can provide a hemodynamic assessment of LA systolic function. (+info)The pulmonary venous systolic flow pulse--its origin and relationship to left atrial pressure. (8/343)
OBJECTIVES: The purpose of this study was to determine the origin of the pulmonary venous systolic flow pulse using wave-intensity analysis to separate forward- and backward-going waves. BACKGROUND: The mechanism of the pulmonary venous systolic flow pulse is unclear and could be a "suction effect" due to a fall in atrial pressure (backward-going wave) or a "pushing effect" due to forward-propagation of right ventricular (RV) pressure (forward-going wave). METHODS: In eight patients during coronary surgery, pulmonary venous flow (flow probe), velocity (microsensor) and pressure (micromanometer) were recorded. We calculated wave intensity (dP x dU) as change in pulmonary venous pressure (dP) times change in velocity (dU) at 5 ms intervals. When dP x dU > 0 there is a net forward-going wave and when dP x dU < 0 there is a net backward-going wave. RESULTS: Systolic pulmonary venous flow was biphasic. When flow accelerated in early systole (S1), pulmonary venous pressure was falling, and, therefore, dP x dU was negative, -0.6 +/- 0.2 (x +/- SE) W/m2, indicating a net backward-going wave. When flow accelerated in late systole (S2), pressure was rising, and, therefore, dP x dU was positive, 0.3 +/- 0.1 W/m2, indicating a net forward-going wave. CONCLUSIONS: Pulmonary venous flow acceleration in S1 was attributed to a net backward-going wave secondary to a fall in atrial pressure. However, flow acceleration in S2 was attributed to a net forward-going wave, consistent with propagation of the RV systolic pressure pulse across the lungs. Pulmonary vein systolic flow pattern, therefore, appears to be determined by right- as well as left-sided cardiac events. (+info)Left atrial function refers to the role and performance of the left atrium in the heart. The left atrium is the upper chamber on the left side of the heart that receives oxygenated blood from the lungs via the pulmonary veins and then contracts to help pump it into the left ventricle, which is the lower chamber that pumps blood out to the rest of the body.
The main functions of the left atrium include:
1. Receiving oxygen-rich blood from the lungs: The left atrium receives oxygenated blood from the pulmonary veins and acts as a reservoir for this blood before it is pumped into the left ventricle.
2. Contracting to help pump blood into the left ventricle: During atrial contraction, also known as atrial kick, the left atrium contracts and helps push blood into the left ventricle, increasing the amount of blood that can be ejected with each heartbeat.
3. Relaxing to receive more blood: Between heartbeats, the left atrium relaxes and fills up with more oxygenated blood from the lungs.
4. Contributing to heart rate regulation: The left atrium contains specialized cells called pacemaker cells that can help regulate the heart rate by initiating electrical impulses that trigger heart contractions.
Left atrial function is crucial for maintaining efficient cardiac output and overall cardiovascular health. Various conditions, such as heart failure, atrial fibrillation, and hypertension, can negatively impact left atrial function and contribute to the development of complications like stroke and reduced exercise tolerance.
Atrial function in a medical context refers to the role and performance of the two upper chambers of the heart, known as the atria. The main functions of the atria are to receive blood from the veins and help pump it into the ventricles, which are the lower pumping chambers of the heart.
The atria contract in response to electrical signals generated by the sinoatrial node, which is the heart's natural pacemaker. This contraction helps to fill the ventricles with blood before they contract and pump blood out to the rest of the body. Atrial function can be assessed through various diagnostic tests, such as echocardiograms or electrocardiograms (ECGs), which can help identify any abnormalities in atrial structure or electrical activity that may affect heart function.
Right atrial function refers to the role and performance of the right atrium in the heart. The right atrium is one of the four chambers of the heart and is responsible for receiving deoxygenated blood from the body via the superior and inferior vena cava. It then contracts to help pump the blood into the right ventricle, which subsequently sends it to the lungs for oxygenation.
Right atrial function can be assessed through various methods, including echocardiography, cardiac magnetic resonance imaging (MRI), and electrocardiogram (ECG). Abnormalities in right atrial function may indicate underlying heart conditions such as right-sided heart failure, atrial fibrillation, or other cardiovascular diseases. Proper evaluation and monitoring of right atrial function are essential for effective diagnosis, treatment, and management of these conditions.
The heart atria are the upper chambers of the heart that receive blood from the veins and deliver it to the lower chambers, or ventricles. There are two atria in the heart: the right atrium receives oxygen-poor blood from the body and pumps it into the right ventricle, which then sends it to the lungs to be oxygenated; and the left atrium receives oxygen-rich blood from the lungs and pumps it into the left ventricle, which then sends it out to the rest of the body. The atria contract before the ventricles during each heartbeat, helping to fill the ventricles with blood and prepare them for contraction.
Atrial fibrillation (A-tre-al fi-bru-la'shun) is a type of abnormal heart rhythm characterized by rapid and irregular beating of the atria, the upper chambers of the heart. In this condition, the electrical signals that coordinate heartbeats don't function properly, causing the atria to quiver instead of contracting effectively. As a result, blood may not be pumped efficiently into the ventricles, which can lead to blood clots, stroke, and other complications. Atrial fibrillation is a common type of arrhythmia and can cause symptoms such as palpitations, shortness of breath, fatigue, and dizziness. It can be caused by various factors, including heart disease, high blood pressure, age, and genetics. Treatment options include medications, electrical cardioversion, and surgical procedures to restore normal heart rhythm.
Doppler echocardiography is a type of ultrasound test that uses high-frequency sound waves to produce detailed images of the heart and its blood vessels. It measures the direction and speed of blood flow in the heart and major blood vessels leading to and from the heart. This helps to evaluate various conditions such as valve problems, congenital heart defects, and heart muscle diseases.
In Doppler echocardiography, a small handheld device called a transducer is placed on the chest, which emits sound waves that bounce off the heart and blood vessels. The transducer then picks up the returning echoes, which are processed by a computer to create moving images of the heart.
The Doppler effect is used to measure the speed and direction of blood flow. This occurs when the frequency of the sound waves changes as they bounce off moving objects, such as red blood cells. By analyzing these changes, the ultrasound machine can calculate the velocity and direction of blood flow in different parts of the heart.
Doppler echocardiography is a non-invasive test that does not require any needles or dyes. It is generally safe and painless, although patients may experience some discomfort from the pressure applied by the transducer on the chest. The test usually takes about 30 to 60 minutes to complete.
Echocardiography, Doppler, pulsed is a type of diagnostic medical test that uses ultrasound to create detailed images of the heart's structures and assess their function. In this technique, high-frequency sound waves are directed at the heart using a handheld device called a transducer, which is placed on the chest wall. The sound waves bounce off the heart structures and return to the transducer, which then sends the information to a computer that converts it into images.
Pulsed Doppler echocardiography is a specific type of Doppler ultrasound that allows for the measurement of blood flow velocities in the heart and great vessels. In this technique, the transducer emits short bursts or "pulses" of sound waves and then measures the time it takes for the echoes to return. By analyzing the frequency shifts of the returning echoes, the velocity and direction of blood flow can be determined. This information is particularly useful in evaluating valvular function, assessing the severity of valvular lesions, and identifying areas of turbulent or abnormal blood flow.
Overall, echocardiography, Doppler, pulsed is a valuable tool for diagnosing and managing a wide range of cardiovascular conditions, including heart valve disorders, congenital heart defects, cardiomyopathies, and pericardial diseases.
Pericardiectomy is a surgical procedure that involves the removal of all or part of the pericardium, which is the sac-like membrane surrounding the heart. This surgery is typically performed to treat chronic or recurrent pericarditis, constrictive pericarditis, or pericardial effusions that do not respond to other treatments. Pericardiectomy can help reduce symptoms such as chest pain, shortness of breath, and fluid buildup around the heart, improving the patient's quality of life and overall prognosis.
Electric countershock, also known as defibrillation, is a medical procedure that uses an electric current to restore normal heart rhythm in certain types of cardiac arrhythmias, such as ventricular fibrillation or pulseless ventricular tachycardia. The procedure involves delivering a therapeutic dose of electrical energy to the heart through electrodes placed on the chest wall or directly on the heart. This electric current helps to depolarize a large number of cardiac cells simultaneously, which can help to interrupt the abnormal electrical activity in the heart and allow the normal conduction system to regain control and restore a normal rhythm. Electric countershock is typically delivered using an automated external defibrillator (AED) or a manual defibrillator, and it is a critical component of advanced cardiac life support (ACLS).
Left ventricular function refers to the ability of the left ventricle (the heart's lower-left chamber) to contract and relax, thereby filling with and ejecting blood. The left ventricle is responsible for pumping oxygenated blood to the rest of the body. Its function is evaluated by measuring several parameters, including:
1. Ejection fraction (EF): This is the percentage of blood that is pumped out of the left ventricle with each heartbeat. A normal ejection fraction ranges from 55% to 70%.
2. Stroke volume (SV): The amount of blood pumped by the left ventricle in one contraction. A typical SV is about 70 mL/beat.
3. Cardiac output (CO): The total volume of blood that the left ventricle pumps per minute, calculated as the product of stroke volume and heart rate. Normal CO ranges from 4 to 8 L/minute.
Assessment of left ventricular function is crucial in diagnosing and monitoring various cardiovascular conditions such as heart failure, coronary artery disease, valvular heart diseases, and cardiomyopathies.
Myocardial contraction refers to the rhythmic and forceful shortening of heart muscle cells (myocytes) in the myocardium, which is the muscular wall of the heart. This process is initiated by electrical signals generated by the sinoatrial node, causing a wave of depolarization that spreads throughout the heart.
During myocardial contraction, calcium ions flow into the myocytes, triggering the interaction between actin and myosin filaments, which are the contractile proteins in the muscle cells. This interaction causes the myofilaments to slide past each other, resulting in the shortening of the sarcomeres (the functional units of muscle contraction) and ultimately leading to the contraction of the heart muscle.
Myocardial contraction is essential for pumping blood throughout the body and maintaining adequate circulation to vital organs. Any impairment in myocardial contractility can lead to various cardiac disorders, such as heart failure, cardiomyopathy, and arrhythmias.
Echocardiography is a medical procedure that uses sound waves to produce detailed images of the heart's structure, function, and motion. It is a non-invasive test that can help diagnose various heart conditions, such as valve problems, heart muscle damage, blood clots, and congenital heart defects.
During an echocardiogram, a transducer (a device that sends and receives sound waves) is placed on the chest or passed through the esophagus to obtain images of the heart. The sound waves produced by the transducer bounce off the heart structures and return to the transducer, which then converts them into electrical signals that are processed to create images of the heart.
There are several types of echocardiograms, including:
* Transthoracic echocardiography (TTE): This is the most common type of echocardiogram and involves placing the transducer on the chest.
* Transesophageal echocardiography (TEE): This type of echocardiogram involves passing a specialized transducer through the esophagus to obtain images of the heart from a closer proximity.
* Stress echocardiography: This type of echocardiogram is performed during exercise or medication-induced stress to assess how the heart functions under stress.
* Doppler echocardiography: This type of echocardiogram uses sound waves to measure blood flow and velocity in the heart and blood vessels.
Echocardiography is a valuable tool for diagnosing and managing various heart conditions, as it provides detailed information about the structure and function of the heart. It is generally safe, non-invasive, and painless, making it a popular choice for doctors and patients alike.
Heart function tests are a group of diagnostic exams that are used to evaluate the structure and functioning of the heart. These tests help doctors assess the pumping efficiency of the heart, the flow of blood through the heart, the presence of any heart damage, and the overall effectiveness of the heart in delivering oxygenated blood to the rest of the body.
Some common heart function tests include:
1. Echocardiogram (Echo): This test uses sound waves to create detailed images of the heart's structure and functioning. It can help detect any damage to the heart muscle, valves, or sac surrounding the heart.
2. Nuclear Stress Test: This test involves injecting a small amount of radioactive substance into the patient's bloodstream and taking images of the heart while it is at rest and during exercise. The test helps evaluate blood flow to the heart and detect any areas of reduced blood flow, which could indicate coronary artery disease.
3. Cardiac Magnetic Resonance Imaging (MRI): This test uses magnetic fields and radio waves to create detailed images of the heart's structure and function. It can help detect any damage to the heart muscle, valves, or other structures of the heart.
4. Electrocardiogram (ECG): This test measures the electrical activity of the heart and helps detect any abnormalities in the heart's rhythm or conduction system.
5. Exercise Stress Test: This test involves walking on a treadmill or riding a stationary bike while being monitored for changes in heart rate, blood pressure, and ECG readings. It helps evaluate exercise capacity and detect any signs of coronary artery disease.
6. Cardiac Catheterization: This is an invasive procedure that involves inserting a catheter into the heart to measure pressures and take samples of blood from different parts of the heart. It can help diagnose various heart conditions, including heart valve problems, congenital heart defects, and coronary artery disease.
Overall, heart function tests play an essential role in diagnosing and managing various heart conditions, helping doctors provide appropriate treatment and improve patient outcomes.
Transesophageal echocardiography (TEE) is a type of echocardiogram, which is a medical test that uses sound waves to create detailed images of the heart. In TEE, a special probe containing a transducer is passed down the esophagus (the tube that connects the mouth to the stomach) to obtain views of the heart from behind. This allows for more detailed images of the heart structures and function compared to a standard echocardiogram, which uses a probe placed on the chest. TEE is often used in patients with poor image quality from a standard echocardiogram or when more detailed images are needed to diagnose or monitor certain heart conditions. It is typically performed by a trained cardiologist or sonographer under the direction of a cardiologist.
Ventricular function, in the context of cardiac medicine, refers to the ability of the heart's ventricles (the lower chambers) to fill with blood during the diastole phase and eject blood during the systole phase. The ventricles are primarily responsible for pumping oxygenated blood out to the body (left ventricle) and deoxygenated blood to the lungs (right ventricle).
There are several ways to assess ventricular function, including:
1. Ejection Fraction (EF): This is the most commonly used measure of ventricular function. It represents the percentage of blood that is ejected from the ventricle during each heartbeat. A normal left ventricular ejection fraction is typically between 55% and 70%.
2. Fractional Shortening (FS): This is another measure of ventricular function, which calculates the change in size of the ventricle during contraction as a percentage of the original size. A normal FS for the left ventricle is typically between 25% and 45%.
3. Stroke Volume (SV): This refers to the amount of blood that is pumped out of the ventricle with each heartbeat. SV is calculated by multiplying the ejection fraction by the end-diastolic volume (the amount of blood in the ventricle at the end of diastole).
4. Cardiac Output (CO): This is the total amount of blood that the heart pumps in one minute. It is calculated by multiplying the stroke volume by the heart rate.
Impaired ventricular function can lead to various cardiovascular conditions, such as heart failure, cardiomyopathy, and valvular heart disease. Assessing ventricular function is crucial for diagnosing these conditions, monitoring treatment response, and guiding clinical decision-making.
Stroke volume is a term used in cardiovascular physiology and medicine. It refers to the amount of blood that is pumped out of the left ventricle of the heart during each contraction (systole). Specifically, it is the difference between the volume of blood in the left ventricle at the end of diastole (when the ventricle is filled with blood) and the volume at the end of systole (when the ventricle has contracted and ejected its contents into the aorta).
Stroke volume is an important measure of heart function, as it reflects the ability of the heart to pump blood effectively to the rest of the body. A low stroke volume may indicate that the heart is not pumping efficiently, while a high stroke volume may suggest that the heart is working too hard. Stroke volume can be affected by various factors, including heart disease, high blood pressure, and physical fitness level.
The formula for calculating stroke volume is:
Stroke Volume = End-Diastolic Volume - End-Systolic Volume
Where end-diastolic volume (EDV) is the volume of blood in the left ventricle at the end of diastole, and end-systolic volume (ESV) is the volume of blood in the left ventricle at the end of systole.
Observer variation, also known as inter-observer variability or measurement agreement, refers to the difference in observations or measurements made by different observers or raters when evaluating the same subject or phenomenon. It is a common issue in various fields such as medicine, research, and quality control, where subjective assessments are involved.
In medical terms, observer variation can occur in various contexts, including:
1. Diagnostic tests: Different radiologists may interpret the same X-ray or MRI scan differently, leading to variations in diagnosis.
2. Clinical trials: Different researchers may have different interpretations of clinical outcomes or adverse events, affecting the consistency and reliability of trial results.
3. Medical records: Different healthcare providers may document medical histories, physical examinations, or treatment plans differently, leading to inconsistencies in patient care.
4. Pathology: Different pathologists may have varying interpretations of tissue samples or laboratory tests, affecting diagnostic accuracy.
Observer variation can be minimized through various methods, such as standardized assessment tools, training and calibration of observers, and statistical analysis of inter-rater reliability.
Blood flow velocity is the speed at which blood travels through a specific part of the vascular system. It is typically measured in units of distance per time, such as centimeters per second (cm/s) or meters per second (m/s). Blood flow velocity can be affected by various factors, including cardiac output, vessel diameter, and viscosity of the blood. Measuring blood flow velocity is important in diagnosing and monitoring various medical conditions, such as heart disease, stroke, and peripheral vascular disease.
Hemodynamics is the study of how blood flows through the cardiovascular system, including the heart and the vascular network. It examines various factors that affect blood flow, such as blood volume, viscosity, vessel length and diameter, and pressure differences between different parts of the circulatory system. Hemodynamics also considers the impact of various physiological and pathological conditions on these variables, and how they in turn influence the function of vital organs and systems in the body. It is a critical area of study in fields such as cardiology, anesthesiology, and critical care medicine.
Left ventricular dysfunction (LVD) is a condition characterized by the impaired ability of the left ventricle of the heart to pump blood efficiently during contraction. The left ventricle is one of the four chambers of the heart and is responsible for pumping oxygenated blood to the rest of the body.
LVD can be caused by various underlying conditions, such as coronary artery disease, cardiomyopathy, valvular heart disease, or hypertension. These conditions can lead to structural changes in the left ventricle, including remodeling, hypertrophy, and dilation, which ultimately impair its contractile function.
The severity of LVD is often assessed by measuring the ejection fraction (EF), which is the percentage of blood that is pumped out of the left ventricle during each contraction. A normal EF ranges from 55% to 70%, while an EF below 40% is indicative of LVD.
LVD can lead to various symptoms, such as shortness of breath, fatigue, fluid retention, and decreased exercise tolerance. It can also increase the risk of complications, such as heart failure, arrhythmias, and cardiac arrest. Treatment for LVD typically involves managing the underlying cause, along with medications to improve contractility, reduce fluid buildup, and control heart rate. In severe cases, devices such as implantable cardioverter-defibrillators (ICDs) or left ventricular assist devices (LVADs) may be required.
Left ventricular hypertrophy (LVH) is a medical condition in which the left ventricle of the heart undergoes an enlargement or thickening of its muscle wall. The left ventricle is the main pumping chamber of the heart that supplies oxygenated blood to the rest of the body.
In response to increased workload, such as hypertension (high blood pressure), aortic valve stenosis, or athletic training, the left ventricular muscle may thicken and enlarge. This process is called "hypertrophy." While some degree of hypertrophy can be adaptive in athletes, significant or excessive hypertrophy can lead to impaired relaxation and filling of the left ventricle during diastole, reduced pumping capacity, and decreased compliance of the chamber.
Left ventricular hypertrophy is often asymptomatic initially but can increase the risk of various cardiovascular complications such as heart failure, arrhythmias, myocardial infarction (heart attack), and sudden cardiac death over time. It is typically diagnosed through imaging techniques like echocardiography or cardiac MRI and confirmed by measuring the thickness of the left ventricular wall.
Feline arterial thromboembolism
Left Atrial Phasic Function Remodeling During Its Enlargement: a Two-dimensional Speckle-tracking Echocardiography Study |...
The Effect of Renal Denervation on Cardiac Diastolic Function in Patients with Hypertension and Paroxysmal Atrial Fibrillation
Relation of atrial natriuretic pepitdes to left ventricular systolic and diastolic function in heart failure<...
Assessment of left atrial functions in cardiac syndrome X | AVESİS
Chromosome 4q25 Variant rs6817105 Bring Sinus Node Dysfunction and Left Atrial Enlargement | Scientific Reports
Left atrial function assessed by left atrial strain in patients with left circumflex branch culprit acute myocardial infarction...
ESC 365 - Left ventricular diastolic function is a determinant of the left atrial mechanics in systemic sclerosis
Effect of pimobendan on left atrial function in dogs with preclinical myxomatous mitral valve disease | Open Veterinary Journal
Reference values of left atrial size and function according to age: should we redefine the normal upper limits?
History The arrhythmic function from the still left atrial appendage (LAA) - Long-term outcome after resection of brainstem...
Atrial Tachycardia: Practice Essentials, Background, Anatomy![Parkash R[au] - Search Results - PubMed](data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAABAAAAAQCAMAAAAoLQ9TAAAARVBMVEVHcEwoU45gYmYAUpQAUpRPYGVgYmZLXnJgYmYAUZUAUpRJXnIAUpQAUpRgYmYAUpRgYmZgYmZhYmYAUpQAUpQAUpRgYmaDiPJuAAAAFXRSTlMADOJ+6QewGO8/uTRqtH7GdFJ11p1bCL3TAAAAZUlEQVQYlV2PVw7AIAxDTeney7n/UcsoldX3E+VJOAboEi7MBpHWMs1ADlG8u7UYWauwyZFeRQVPOhG2o+aiwhByJxUx91Jxhje3iJSqGfHuLKI0+0TpXvY1twCOPlFh5pa/++MB0vIOBm+1zaoAAAAASUVORK5CYII=)
Parkash R[au] - Search Results - PubMed
Michael Henein
Bjarne Martens Nes - NTNU
Stanley Loriston - Articles - Scientific Research Publishing
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