Cardiovascular
Cardiac Output
December 05, 2009, 19:41
Cardiac Output Measurement
By Donald R. Elton, MD, FCCP
Lexington Pulmonary and Critical Care
Introduction
Cardiac output is the amount of blood ejected from the left ventricle in one minute and is measured in liters per minute. Under normal circumstances, the outputs of the left and right ventricles must be equal in the absence of abnormal shunts between the pulmonary and systemic circulatory systems.
Physiology
Along with left ventricular filling pressures (pulmonary capillary wedge pressure), the cardiac output is one of the few hemodynamic parameters that with today's technology requires the placement of a pulmonary artery catheter. Cardiac output is the product of heart rate and stroke volume. Heart rate is determined by both intrinsic pacemaker function and modulation by the autonomic nervous system. Stroke volume is dependent upon the degree of diastolic ventricular filling coupled with the degree of contraction sometimes expressed as ejection fraction. Disease states can alter all of these components of cardiac output. Normally, as heart rate increases, the cardiac output increases proportionately. As heart rate increases however, the time available for ventricular filling to occur decreases and in each patient, there is a heart rate, above which, ventricular filling will decrease enough that further increases in heart rate will result in a lowered cardiac output. In a normal person, this cut-off occurs somewhere between 180-200 beats per minute while in disease states such as congestive heart failure secondary to cardiomyopathy, this cut-off may be reached at rates as low as 120 beats per minute. Uncontrolled atrial fibrillation or atrial flutter frequently result in heart rates that are too high for adequate cardiac output and a major part of the treatment of these arrythmias is to give the patient digoxin to help slow the abnormally high heart rate.
Measurement Methods
Two main methods are used to measure cardiac output today. These are the Fick method and dilution methods (either dye or thermal).
Fick Method
The Fick method requires that you be able to measure the A-V oxygen content difference and requires that you be able to measure the oxygen consumption. An arterial blood gas from a peripheral artery provides the blood for the CaO2 measurement or calculation while blood from the distal PA port of a Swan-Ganz catheter provides the blood for the CvO2 measurement or calculation. Oxygen consumption is obtained by measuring the inspired oxygen concentration and the expired oxygen concentration along with the expired minute volume. Small errors in the oxygen concentration measurements can result in large mathematical errors therefore these measurements should be made with a calibrated blood gas machine equipped for measurement of gas samples (such as the ABL 300, IL, or Corning blood gas machines). Note the Fick cardiac output formula from a previous lecture. Fick cardiac outputs are infrequently used mainly because of the inconvenience of collecting and analyzing exhaled gas concentrations. It's not as difficult to do as one might think but nonetheless Fick cardiac outputs are seldom used today. You may see mention of an estimated Fick cardiac output method where you just assume that oxygen consumption is normal by plucking a value off of a nomagram corrected for weight and height but in patients in whom a cardiac output determination is really needed, the oxygen consumption is seldom normal and these estimated cardiac output measurements can do more harm than good.
Dilution Methods
Dilution methods mathematically calculate (using calculus) the cardiac output based on how fast the flowing blood can dilute a marker substance introduced into the circulation normally via a pulmonary artery catheter. The marker must be distinguishable from the blood and must be able to be measured quickly and with a high degree of accuracy. Early dilution methods used dye solutions which were administered upstream and then drawn off in blood samples downstream from the infusion port where they could be analyzed for concentration. Cardiac output was inversely related to the downstream dye concentration. Dye dilution cardiac outputs are seldom used today outside of cardiac catheterization labs and even most of them use the more automated thermal dilution method. In thermal dilution, cold or room temperature water or D5W is used as the marker solution and distal concentration is determined by measuring the temperature downstream from the infusion port. Since water is non-toxic, multiple measurements can be made as often as needed and the downstream concentration (i.e. temperature) can be measured in situ without having to withdraw any blood from the circulation for analysis.
Errors
Cardiac output measurement is not precise using today's technology. For clinical use, we don't need 100% accuracy to 5 significant digits but to avoid big errors it is important to know the limitations of the measurement techniques. Fick cardiac output errors result from leaky gas collection apparatus, from inaccuracies in the measurement of inhaled and exhaled oxygen concentrations (these are particularly common when high levels of oxygen are used), an from errors in the calculations and/or measurements of blood oxygen contents (such as might be caused by using a bogus hemoglobin level or assuming the absence of carbon monoxide affecting oxygen saturation). Thermal dilution cardiac outputs are affected by the phase of respiration, particularly during mechanical ventilation and should thus always be measured at the same point in the respiratory cycle (normally end-expiratory) where the effect of breathing (either spontaneous or mechanical) is least. Small errors can result from using the wrong fluid (something other than D5W) as the injectate. Variations in the speed of cold water injection can result in altered measurements and devices to automatically inject the fluid are available to eliminate this source of variation. While there are lots of things that can result in cardiac output measurements not exactly equaling the true cardiac output, the most important concept here is to make the measurements reproducible and the errors consistent from one measurement to the next. It is the change in cardiac output, up or down, that allows the practitioner to determine the effects of therapy and disease and not the absolute value but to accurately detect changes, the output measurement errors must be consistent.
By Donald R. Elton, MD, FCCP
Lexington Pulmonary and Critical Care
Introduction
Cardiac output is the amount of blood ejected from the left ventricle in one minute and is measured in liters per minute. Under normal circumstances, the outputs of the left and right ventricles must be equal in the absence of abnormal shunts between the pulmonary and systemic circulatory systems.
Physiology
Along with left ventricular filling pressures (pulmonary capillary wedge pressure), the cardiac output is one of the few hemodynamic parameters that with today's technology requires the placement of a pulmonary artery catheter. Cardiac output is the product of heart rate and stroke volume. Heart rate is determined by both intrinsic pacemaker function and modulation by the autonomic nervous system. Stroke volume is dependent upon the degree of diastolic ventricular filling coupled with the degree of contraction sometimes expressed as ejection fraction. Disease states can alter all of these components of cardiac output. Normally, as heart rate increases, the cardiac output increases proportionately. As heart rate increases however, the time available for ventricular filling to occur decreases and in each patient, there is a heart rate, above which, ventricular filling will decrease enough that further increases in heart rate will result in a lowered cardiac output. In a normal person, this cut-off occurs somewhere between 180-200 beats per minute while in disease states such as congestive heart failure secondary to cardiomyopathy, this cut-off may be reached at rates as low as 120 beats per minute. Uncontrolled atrial fibrillation or atrial flutter frequently result in heart rates that are too high for adequate cardiac output and a major part of the treatment of these arrythmias is to give the patient digoxin to help slow the abnormally high heart rate.
Measurement Methods
Two main methods are used to measure cardiac output today. These are the Fick method and dilution methods (either dye or thermal).
Fick Method
The Fick method requires that you be able to measure the A-V oxygen content difference and requires that you be able to measure the oxygen consumption. An arterial blood gas from a peripheral artery provides the blood for the CaO2 measurement or calculation while blood from the distal PA port of a Swan-Ganz catheter provides the blood for the CvO2 measurement or calculation. Oxygen consumption is obtained by measuring the inspired oxygen concentration and the expired oxygen concentration along with the expired minute volume. Small errors in the oxygen concentration measurements can result in large mathematical errors therefore these measurements should be made with a calibrated blood gas machine equipped for measurement of gas samples (such as the ABL 300, IL, or Corning blood gas machines). Note the Fick cardiac output formula from a previous lecture. Fick cardiac outputs are infrequently used mainly because of the inconvenience of collecting and analyzing exhaled gas concentrations. It's not as difficult to do as one might think but nonetheless Fick cardiac outputs are seldom used today. You may see mention of an estimated Fick cardiac output method where you just assume that oxygen consumption is normal by plucking a value off of a nomagram corrected for weight and height but in patients in whom a cardiac output determination is really needed, the oxygen consumption is seldom normal and these estimated cardiac output measurements can do more harm than good.
Dilution Methods
Dilution methods mathematically calculate (using calculus) the cardiac output based on how fast the flowing blood can dilute a marker substance introduced into the circulation normally via a pulmonary artery catheter. The marker must be distinguishable from the blood and must be able to be measured quickly and with a high degree of accuracy. Early dilution methods used dye solutions which were administered upstream and then drawn off in blood samples downstream from the infusion port where they could be analyzed for concentration. Cardiac output was inversely related to the downstream dye concentration. Dye dilution cardiac outputs are seldom used today outside of cardiac catheterization labs and even most of them use the more automated thermal dilution method. In thermal dilution, cold or room temperature water or D5W is used as the marker solution and distal concentration is determined by measuring the temperature downstream from the infusion port. Since water is non-toxic, multiple measurements can be made as often as needed and the downstream concentration (i.e. temperature) can be measured in situ without having to withdraw any blood from the circulation for analysis.
Errors
Cardiac output measurement is not precise using today's technology. For clinical use, we don't need 100% accuracy to 5 significant digits but to avoid big errors it is important to know the limitations of the measurement techniques. Fick cardiac output errors result from leaky gas collection apparatus, from inaccuracies in the measurement of inhaled and exhaled oxygen concentrations (these are particularly common when high levels of oxygen are used), an from errors in the calculations and/or measurements of blood oxygen contents (such as might be caused by using a bogus hemoglobin level or assuming the absence of carbon monoxide affecting oxygen saturation). Thermal dilution cardiac outputs are affected by the phase of respiration, particularly during mechanical ventilation and should thus always be measured at the same point in the respiratory cycle (normally end-expiratory) where the effect of breathing (either spontaneous or mechanical) is least. Small errors can result from using the wrong fluid (something other than D5W) as the injectate. Variations in the speed of cold water injection can result in altered measurements and devices to automatically inject the fluid are available to eliminate this source of variation. While there are lots of things that can result in cardiac output measurements not exactly equaling the true cardiac output, the most important concept here is to make the measurements reproducible and the errors consistent from one measurement to the next. It is the change in cardiac output, up or down, that allows the practitioner to determine the effects of therapy and disease and not the absolute value but to accurately detect changes, the output measurement errors must be consistent.
Aortic Dissection
December 05, 2009, 19:39
Aortic Dissection
By Donald R. Elton, MD, FCCP
Lexington Pulmonary and Critical Care
Introduction
Aortic dissection is a potentially lethal condition that is the most common acute catastrophe involving the Aorta. It occurs two to three times more frequently than rupture of abdominal aortic aneurysms.
Etiology
The pathogenesis of aortic dissection is not completely understood. It was once thought that a condition known as cystic medial necrosis, a pathological condition of uncertain cause, had to exist along with an intimal tear before a dissection could occur. It is now known that what was once called cystic medial necrosis is a normal part of aging of the Aorta. One thing that is clear is that hypertension is related to aortic dissection. The peak incidence is between 50 and 70 years of age. Dissections are slightly more common in men and in patients who have Marfan's syndrome. Pregnancy is a rare predisposing condition.
Classification
There are two major classification systems for aortic dissections and both are based upon the location of the dissection. The vast majority of aortic dissections occur either at the ascending aorta just above the aortic valve or occur just below the origin of the left subclavian artery. The DeBakey classification calls a Type I dissection one in which the tear originates in the ascending aorta and dissects into the descending aorta. A Type II dissection originates in and is limited to the ascending aorta. A Type III dissection originates in the descending aorta and may progress in either direction. More recently, the Austen and Shumway classification divides dissections into Type A and Type B for ascending and descending dissections respectively.
Pathophysiology
Aortic dissections cause death and morbidity by any or all of several mechanisms. Depending on the location of the dissection, there can be disruption of any of the major branches off of the aorta leading to ischemic injury in the area of distribution of the involved vessels such as the carotids, renals, or coronary arteries. Dissection of the ascending aorta can distort the aortic valve resulting in acute life-threatening aortic insufficiency with resultant congestive heart failure. Thrombi can form and result in distal arterial obstruction in the lower extremities. Exsanguination can occur if the false lumen of the Aorta bleeds into the pleural space or mediastinum and pericardial tamponade can occur if blood dissects into the pericardium. Frequently the systemic blood pressure, particularly proximal to a major aortic obstruction can be very high and very labile and this can result in cerebrovascular accidents.
Presentation
Severe acute chest pain occurs in 95% of patients with aortic dissection. The pain is typically sudden in onset and has a sharp tearing or throbbing quality. The pain is usually centered in the sub sternal region but may be felt in the jaw, precordium, neck, jaw, extremities, epigastrium, or back. Depending on complications there may be neurologic deficits and or evidence of ischemia elsewhere such as blindness or extremity pain. If aortic insufficiency occurs then evidence of acute heart failure may result leading to the appearance of an acute myocardial infarction. Of course, an acute myocardial infarction can also occur because of disruption of a coronary artery at its origin in the proximal aorta. Physical findings vary from shock, to hypertension, to heart failure. Sequential filling of the true and false lumens may produce "double" pulses and there may be unequal blood pressures in the extremities if compromise of the distal artery has ocurred.
Diagnosis
The chest x-ray frequently shows a widened superior mediastinum representing either a mediastinal hematoma or a widened aortic shadow. The initial x-ray may be normal. CT and MRI scanning are fairly specific for aortic dissection and echocardiography, particularly using an esophageal probe can confirm the diagnosis if the area of dissection can be visualized but a negative echocardiogram is not adequate to rule out dissection. Aortography is considered to be the gold standard.
Therapy
Because aortic dissections are life-threatening, specific therapy must be initiated very quickly in many cases. Therapy should not be delayed for aortography if the diagnosis is already apparent. Immediate therapy is aimed at both reducing the blood pressure and at reducing the pulsatile force of left ventricular ejection. Typically, a combination of nitroprusside (Nipride) and propranolol (Inderal) are used to accomplish both goals. Trimethophan camsylate (Arfonad), a ganglionic blocking agent can also be used both to lower the blood pressure and lower the force of left ventricular contraction. Blood pressure should be lowered to the lowest pressure that maintains cerebral and renal perfusion. Definitive surgical repair is indicated for all proximal dissections and for distal dissections with complications (i.e. bleeding, vascular obstruction) while medical therapy is preferred for uncomplicated acute or chronic distal dissections. Repair of proximal dissections may require repair and/or replacement of the aortic valve as well as coronary revascularization.
Outcome
Half of patients with untreated thoracic aortic dissections die within 48 hours and 90% do not survive 6 months. A compilation of the literature in 1983 revealed that for treated type A dissections, medical treatment had a 72% mortality while surgical treatment had a 32% mortality. For type B dissections, medical treatment had a 27% mortality while surgical treatment had a 32% mortality. Ten year survival is around 20% for either type of dissection.
References
Little AG, Anagnostopoulos CE: Aortic Dissections in Thoracic and Cardiovascular Surgery, 4th Edition, Editor W. Glenn, 1983, Appleton-Century-Crofts.
Thompson WL: Hypertensive Urgencies and Emergencies in Textbook of Critical Care, 2nd Edition, Editor Shoemaker et al, 1989, W. B. Saunders Company.
DeBakey ME, Cooley DA, Creech O Jr: Surgical consideration of dissecting aneurysm of the aorta. Ann Surg 142:586, 1955.
By Donald R. Elton, MD, FCCP
Lexington Pulmonary and Critical Care
Introduction
Aortic dissection is a potentially lethal condition that is the most common acute catastrophe involving the Aorta. It occurs two to three times more frequently than rupture of abdominal aortic aneurysms.
Etiology
The pathogenesis of aortic dissection is not completely understood. It was once thought that a condition known as cystic medial necrosis, a pathological condition of uncertain cause, had to exist along with an intimal tear before a dissection could occur. It is now known that what was once called cystic medial necrosis is a normal part of aging of the Aorta. One thing that is clear is that hypertension is related to aortic dissection. The peak incidence is between 50 and 70 years of age. Dissections are slightly more common in men and in patients who have Marfan's syndrome. Pregnancy is a rare predisposing condition.
Classification
There are two major classification systems for aortic dissections and both are based upon the location of the dissection. The vast majority of aortic dissections occur either at the ascending aorta just above the aortic valve or occur just below the origin of the left subclavian artery. The DeBakey classification calls a Type I dissection one in which the tear originates in the ascending aorta and dissects into the descending aorta. A Type II dissection originates in and is limited to the ascending aorta. A Type III dissection originates in the descending aorta and may progress in either direction. More recently, the Austen and Shumway classification divides dissections into Type A and Type B for ascending and descending dissections respectively.
Pathophysiology
Aortic dissections cause death and morbidity by any or all of several mechanisms. Depending on the location of the dissection, there can be disruption of any of the major branches off of the aorta leading to ischemic injury in the area of distribution of the involved vessels such as the carotids, renals, or coronary arteries. Dissection of the ascending aorta can distort the aortic valve resulting in acute life-threatening aortic insufficiency with resultant congestive heart failure. Thrombi can form and result in distal arterial obstruction in the lower extremities. Exsanguination can occur if the false lumen of the Aorta bleeds into the pleural space or mediastinum and pericardial tamponade can occur if blood dissects into the pericardium. Frequently the systemic blood pressure, particularly proximal to a major aortic obstruction can be very high and very labile and this can result in cerebrovascular accidents.
Presentation
Severe acute chest pain occurs in 95% of patients with aortic dissection. The pain is typically sudden in onset and has a sharp tearing or throbbing quality. The pain is usually centered in the sub sternal region but may be felt in the jaw, precordium, neck, jaw, extremities, epigastrium, or back. Depending on complications there may be neurologic deficits and or evidence of ischemia elsewhere such as blindness or extremity pain. If aortic insufficiency occurs then evidence of acute heart failure may result leading to the appearance of an acute myocardial infarction. Of course, an acute myocardial infarction can also occur because of disruption of a coronary artery at its origin in the proximal aorta. Physical findings vary from shock, to hypertension, to heart failure. Sequential filling of the true and false lumens may produce "double" pulses and there may be unequal blood pressures in the extremities if compromise of the distal artery has ocurred.
Diagnosis
The chest x-ray frequently shows a widened superior mediastinum representing either a mediastinal hematoma or a widened aortic shadow. The initial x-ray may be normal. CT and MRI scanning are fairly specific for aortic dissection and echocardiography, particularly using an esophageal probe can confirm the diagnosis if the area of dissection can be visualized but a negative echocardiogram is not adequate to rule out dissection. Aortography is considered to be the gold standard.
Therapy
Because aortic dissections are life-threatening, specific therapy must be initiated very quickly in many cases. Therapy should not be delayed for aortography if the diagnosis is already apparent. Immediate therapy is aimed at both reducing the blood pressure and at reducing the pulsatile force of left ventricular ejection. Typically, a combination of nitroprusside (Nipride) and propranolol (Inderal) are used to accomplish both goals. Trimethophan camsylate (Arfonad), a ganglionic blocking agent can also be used both to lower the blood pressure and lower the force of left ventricular contraction. Blood pressure should be lowered to the lowest pressure that maintains cerebral and renal perfusion. Definitive surgical repair is indicated for all proximal dissections and for distal dissections with complications (i.e. bleeding, vascular obstruction) while medical therapy is preferred for uncomplicated acute or chronic distal dissections. Repair of proximal dissections may require repair and/or replacement of the aortic valve as well as coronary revascularization.
Outcome
Half of patients with untreated thoracic aortic dissections die within 48 hours and 90% do not survive 6 months. A compilation of the literature in 1983 revealed that for treated type A dissections, medical treatment had a 72% mortality while surgical treatment had a 32% mortality. For type B dissections, medical treatment had a 27% mortality while surgical treatment had a 32% mortality. Ten year survival is around 20% for either type of dissection.
References
Little AG, Anagnostopoulos CE: Aortic Dissections in Thoracic and Cardiovascular Surgery, 4th Edition, Editor W. Glenn, 1983, Appleton-Century-Crofts.
Thompson WL: Hypertensive Urgencies and Emergencies in Textbook of Critical Care, 2nd Edition, Editor Shoemaker et al, 1989, W. B. Saunders Company.
DeBakey ME, Cooley DA, Creech O Jr: Surgical consideration of dissecting aneurysm of the aorta. Ann Surg 142:586, 1955.