Healthy news and views for a long and healthy life…
Hepatoabdominal compression maneuver
The actual simple info with consider to cardiovascular – in advance of we talk pertaining to how a good deal aerobics cardio you must do, you have to at the very least know why it’s so fundamental. Cardiovascular exercising purely signifies that you’re included in an activity that raises your heart rate to a level exactly where you’re working, but can even now discuss (aka, with your Target Heart Rate Zone).
random:50]Cardiac markers new and old
Cardiac markers new and old
Free Online Articles Directory
Why Submit Articles?
Top Authors
Top Articles
FAQ
AB Answers
0 && $.browser.msie ) {
var ie_version = parseInt($.browser.version);
if(ie_version Hello Guest
Login
Register
Hello
My Home
Sign Out
Email
Password
Remember me?
Lost Password?
Home Page > Health > Medicine > Cardiac markers new and old
Cardiac markers new and old
Posted: Nov 19, 2010 |Comments: 0
|
]]>
Ask a question
Ask our experts your Medicine related questions here…200 Characters left
Related Questions
On the coast of Maine is the small town of Pirates Cove it resembles the old New England seaports depicted in paintings hanging in country inns or seafood restaurants
How do you transfer norton antivirus that was renewed on 6/6/10 from an old computer to a new computer?
Can i leave my 3 year old dog alone with my new puppy
I need my old photos of iphoto back. it is lost somewhere and i see new iphoto without any photos. how can i get my all photos back?
Cardiac markers new and old
By: hyder514
About the Author
(ArticlesBase SC #3698627)
Article Source: http://www.articlesbase.com/ – Cardiac markers new and old
Introduction
Cardiac markers or cardiac enzymes are proteins that leak out of injured myocardial cells through their damaged cell membranes into the bloodstream.
They are:
A: specific.
1. Cardiac troponin I and cardiac troponin T
2. Creatine kinase-MB isoenzyme (CK-MB).
B: Non specific.
Until the 1980s, the enzymes SGOT and LDH were used to assess cardiac injury.
1.C-reactive protein
2.B-type natriuretic peptide
3.Copeptin
4.lactate dehydrogenase
5.Aspartatetransferase
6.myoglobin
7.ischemia modified albumin.
8.Glycogen phosphorylase isoenzyme BB.
9.Adiponectin.
10.Adrenomedullin.
A: specific.
1.Cardiac troponin I and cardiac troponin T .
The troponins are part of the actomyosin contractile apparatus of muscle cells. Structurally unique forms of troponin T and troponin I are found in cardiac tissue, enabling the development of immunoassays, which recognise only the cardiac forms of these two proteins. In most clinicalsituations both cardiac troponin I (cTnI) and cardiac troponin T (cTnT) seem to offer similarly useful clinical information.
When a cardiac myocyte dies, CK-MB passes rapidly from the cytoplasm into the circulation and is cleared. In contrast, most of the troponin within the myocyte is found in the structural elements of the cell, so when necrosis occurs there is a steady leaching of troponin into the circulation. Consequently, troponin remains in the circulation for several days after a cardiac event.
Despite extended searching, there is currently no evidence that the cardiac troponins may be produced by tissues other than myocardium. However, the presence of cardiac troponin, while indicating that cardiac injury has occurred, provides no information as to the mechanism of injury. Cardiac troponin concentrations may rise in conditions unrelated to ischaemic damage such as pericarditis, trauma and sepsis. Such rises provide no information about the likelihood of future ischaemic cardiac disease.
When associated with coronary artery ischaemia even low concentrations of cardiac troponin predict an adverse outcome. This is regardless of whether the other WHO criteria for the formal diagnosis of myocardial infarction are met. The pathophysiological mechanism for these acute coronary syndromes is the presence of an unstable coronary plaque, with release of micro-emboli causing focal myocardial necrosis with release of cardiac troponin. The increased mortality is a reflection of a large thrombus separating from the unstable plaque.This improved understanding of the mechanism of the acute coronary syndrome, has led to a proposal to redefine myocardial infarction, using the presence of a cardiac biochemical marker, with some evidence of coronary artery ischaemia, as the central diagnostic criterion.
False positive troponin.
1.Cardiac troponins in patients with renal failure
A small proportion of patients with renal failure undergoing dialysis have detectable concentrations of cTnT. This finding was originally thought to be a false positive test, but careful analysis has shown that these patients do have a worse cardiac prognosis. When one considers that approximately 20% of patients on dialysis die each year and that cardiac disease is the commonest cause of mortality, this result is not unexpected. Although there is some increase in cTnI in dialysis patients, this appears to be one area where cTnT is more informative.
2.Problems with assays for cardiac troponin I
Cardiac troponin I is prone to modification in the circulation. It may be phosphorylated and oxidised and can exist as a complex with either cTnT or cardiac troponin C. This has some clinical relevance, because the different antibodies used in commercial assays may recognise these different molecular forms to varying extents. A major problem with cTnI assays is that the different assays are calibrated with different standards. The same blood sample may give quite different apparent concentrations in different assays. If it is accepted that the presence of any cardiac troponin in the presence of coronary artery ischaemia indicates a worse prognosis, then the absolute concentration is less important.
2.Creatine kinase-MB isoenzyme (CK-MB) .
Creatine kinase (CK) and more particularly its isoenzyme CK-MB still have a formal place in defining myocardial infarction. However the current definition is not a particularly useful one because studies have shown that, as currently defined, patients with myocardial infarction and unstable angina have similar outcomes.
Interpretation of CK-MB is problematic, with both false positives and false negatives occurring. While CK-MB is relatively cardiac-specific, even healthy people may have low concentrations of this isoenzyme in their blood. People with chronic myopathies may have high concentrations of CK-MB because it is produced by regenerating skeletal muscle. A high concentration of CK-MB may therefore be unrelated to cardiac disease (false positive).
The half-life of CK-MB in the circulation is relatively short (approximately 12 hours). Samples collected many hours after an infarction may have both a low absolute concentration of CK-MB and a low ratio of CK-MB to total CK (due to the longer half-life of the major isoenzyme, CK-MM). This can give a false negative result.
Some specialists believe that it is no longer appropriate to use CK-MB in the diagnosis of myocardial infarction. It may be more helpful for investigating possible reinfarction, where its short half-life may be useful compared to the longer time that cardiac troponins spend in the circulation.
B:non specific.
1.C-reactive protein
C-reactive protein (CRP) is an acute phase reactant produced by the liver in response to cytokine release during inflammation. It has long been used in clinical practice to follow systemic inflammation, especially bacterial infection. More recently, epidemiological evidence has shown that basal levels of CRP, in the absence of apparent inflammatory disease (so-called hs-CRP) may be informative in predicting future myocardial or cerebrovascular events.
The value of hs-CRP appears to relate to activity in the atherosclerotic plaque. Amongst the cellular elements of the atherosclerotic plaque are inflammatory cells, which, by releasing interleukin-6, cause secretion of CRP into the circulation. In the Physicians’ Health Study, when people in the highest quartile of CRP values were compared to people with the lowest quartile of CRP values, they had a relative risk of future myocardial infarction of 1.9. In the Women’s Health Study the relative risk was 4.4.
There are a number of problems in using CRP measurements to predict the likelihood of future cardiovascular events. These are both biological and analytical.
Biological variability in basal CRP concentration is considerable. Even mild, subclinical infections can cause significant increases in CRP concentration that are unrelated to cardiovascular disease. For this reason, no measurements should be made within two weeks of any infection. Even with this precaution, CRP concentrations may vary markedly. Several studies have investigated the variability of the CRP concentration in blood collected repeatedly from individuals over periods of weeks to months. The standard deviation for each individual varies from 30% to 63% of the mean value.Thus it might be highly misleading to contemplate using a single measurement to guide possible therapy. It has been proposed that two separate measurements should be made on each individual, while they are quite well, and at intervals of more than a week apart. The lowest value is then used to determine which quartile the person is in. Even this approach may be insufficient to correct for the variability.
There are outstanding laboratory problems with use of hs-CRP. Not all assays produce identical results. No laboratory has the resources to determine its own reference ranges, so transportability of results between assays is obviously of great importance in defining the concentrations that relate to the different quartiles of basal CRP concentration. At the present time it appears undesirable to attempt to use hs-CRP in individual risk stratification.
2 .B-type natriuretic peptide
The cardiac natriuretic peptide family of neuro-endocrine hormones has a complex physiological role in modulating blood volume and pressure. This involves natriuresis and diuresis as well as antagonism to the angiotensin-renin system. These peptides are also antimitotic and may modulate cardiac hypertrophy. In the presence of left ventricular dysfunction, with worsening cardiac failure, the concentration of plasma B-type natriuretic peptide (BNP) increases in proportion to the New York Heart Association’s (NYHA) classification of severity. However, there are a number of other pathophysiological states in which BNP may be elevated, such as hypertension and cardiac hypertrophy, pulmonary hypertension and renal disease. The most appropriate use of this marker remains to be defined.
As with cTnI, several different assays for BNP or its associated peptides (e.g. NT-proBNP) have been used in the published studies. As these assays are not yet standardised, numerical values from one assay cannot be compared quantitatively with those from another.
B-Type Natriuretic Peptide: Prognostic in Heart Failure?
Many patients hospitalized with acute exacerbations of heartfailure are cared for by primary care physicians after discharge.Although some patients avoid rehospitalization within the next6 months, others are prone to multiple hospital admissions.Recently, BNP determinations have shown the potential to bea good prognostic marker for morbidity and mortality in patientswith heart failure, including predicting future cardiac eventin patients with acute exacerbations
One prospective study found that an initial BNP concentrationof 480 pg/mL had a sensitivity of 68%, specificity of 88%, andan accuracy of 85% of predicting a congestive heart failureendpoint (death, hospital admissions, and repeated emergencydepartment visits) after a 6-month follow-up period after hospitaldischarge. Patients with BNP levels greater than 480 pg/mLhad a 51%, 6-month cumulative probability of a heart failureevent (35% of these patients had death from heart failure astheir event), whereas BNP levels of less than 250 pg/mL hada much better prognosis, with only a 2.5% cumulative probabilityof a heart failure event. The authors reported that increasedBNP levels were associated with progressively worse prognosis.
Another well-designed study compared BNP levels with the patient’sheart failure survival score (HFSS), a recognized and acceptedtool in determining a patient’s prognosis. Patientswere classified into three different prognostic groups basedon the HFSS score: low risk, medium risk, or high risk. Therewere significant differences in each group. The mean BNP concentrationfor the low-risk group was 95.7 ± 11.2 pg/mL, for themedium-risk group was 244.4 ± 33.4 pg/mL, and for thehigh-risk group was 419.9 ± 55.5 pg/mL. More importantly,the authors were able to show that higher BNP levels were associatedwith a change in cardiovascular functional class with time.The initial BNP level in patients who improved during the ensuing12 months had a BNP concentration of 42.4 ± 8.6 pg/mL,those who remained stable had a BNP level of 102.2 ±16.1 pg/mL, and those who deteriorated during the ensuing 12months had a BNP level of 256.9 ± 28.5 pg/mL.
B-Type Natriuretic Peptide and Therapeutic Monitoring of Heart Failure
Primary care physicians have the task of managing patients withcongestive heart failure. An important aspect of patient managementis the ability to monitor the therapeutic efficacy of the patient’spharmacological regimen. BNP levels have been found to followventricular function in response to medical management.
One study evaluated left ventricular volume and mass, includingneurohormone levels, in patients with mild to moderate nonischemiccongestive heart failure before and after 4 months of treatmentwith spironolactone or placebo. Patients who received a fixed25-mg dose of spironolactone had a change in their mean BNPconcentration from 200 ± 66 pg/mL at baseline to 89.7± 27 pg/mL at 4 months (P< .01), whereas the controlgroup showed no significant change.
Another study managed to show that BNP-guided treatment of heartfailure reduced total cardiovascular events and delayed timeto first event compared with intensive clinically guided treatment.The BNP concentration decreased 79 pmol/L in the BNP-guidedgroup compared with 3 pmol/L in the clinically-guided group.More importantly, the primary combined clinical endpoint (cardiovasculardeath, hospital admission, and outpatient heart failure) wassignificantly reduced in the BNP-guided group (P< .02).This significance increased when covariates were accounted for(baseline left ventricular ejection fraction, baseline BNP,and medication dosages, New York Heart Association heart failureclass, and systolic blood pressure) in the regression model(P< .001). The authors suggested that BNP-guided treatmentrepresents a preventive strategy targeting more intensive pharmacotherapyand follow-up for patients with elevated circulating BNP levelswho are at high risk of cardiovascular events.
Although both studies describe an important use of BNP, thesmall study sizes should raise caution when applying these findingsto clinical practice
3.Copeptin
Approximately 15 million patients present to the Emergency Department (ED) with symptoms suggestive of Acute Myocardial Infarction (AMI) every year. The vast majority (70 to 80%) of them finally prove not to have AMI. However, due to a delayed increase of circulating levels of Troponin it takes up to six hours before it can be measured. Therefore serial blood sampling is recommended by the European Guidelines. Study results indicate that by testing for both markers, along with an Electrocardiogram (ECG) and the clinical findings, approximately two-thirds of the patients would not need to wait those six hours in the ED for the second Troponin test. This may obviate the need for prolonged monitoring and serial blood sampling in the majority of patients.
“In the very situation of a patient presenting to the Emergency Department (ED) with symptoms suggestive of Acute Myocardial Infarction (AMI) the clinician quickly needs to know whether the person is in real danger or not. Ruling out AMI in this setting is an urgent and unmet need. The use of Copeptin together with Troponin can accelerate the rule out of AMI and thus improves patient management in the ED immensely. Two thirds of these patients may be ruled out with the first blood draw and most of them probably could leave the ED very soon,” explained Dr. Tobias Reichlin from the Department of Internal Medicine at the University Hospital, Basel, Switzerland. While the concentration of Troponin rises four to six hours after the event of an AMI, concentrations of the new Copeptin biomarker are highest right after the onset of symptoms and then begin to drop. This difference makes the use of the combination of the two extremely promising.
The study was conducted in the University Hospital of Basel, Switzerland. In 487 consecutive patients presenting to the Emergency Department (ED) with symptoms suggestive of Acute Myocardial Infarction (AMI), the research team measured levels of copeptin at presentation, using a novel sandwich immunoluminetric assay in a blinded fashion. The final diagnosis was adjudicated by two independent cardiologists using all available data.
The adjudicated final diagnosis was Acute Myocardial Infarction (AMI) in 81 patients (17%). Copeptin levels were significantly higher in AMI patients compared with those in patients having other diagnoses (median 20,8pmol/l vs. 6,0 pmol/l, p<0,001). The combination of Troponin and Copeptin at initial presentation resulted in an area under the receiver-operating characteristic curve of 0,97 (95% confidence interval: 0,95 to 0,98), which was significantly higher than the 0,86 (95% confidence interval: 0,80 to 0,92) for Troponin alone (p<0,001). A Copeptin level < 14 pmol/l in combination with a Troponin ? 0,01 µg/l correctly ruled out AMI with a sensitivity of 98,8% and a negative predictive value of 99,7%.
Copeptin, the C-terminal part of the vasopressin prohormone, is a marker of acute endogenous stress. Arginine vasopressin (AVP) is a key hormone in the human body. Despite the clinical relevance of AVP in maintaining fluid balance and vascular tone, measurement of mature AVP is difficult and subject to preanalytical errors. Recently, Copeptin, a 39-amino acid glycopeptide that comprises the C-terminal part of the AVP precursor (CT-proAVP), was found to be a stable and sensitive surrogate marker for AVP release, analogous to C-peptide for insulin. Copeptin measurement has been shown to be useful in various clinical indications, including the diagnosis of diabetes insipidus and the monitoring of sepsis and cardiovascular diseases.
Copeptin is scheduled for fall introduction on the European market and joins a series of excellent BRAHMS biomarkers for cardiovascular diseases. The study results were already presented in a Late Breaking Clinical Trial Session at the ACC-Meeting in March. It marks the third time in just a few months that BRAHMS, with a new cardiac marker, succeeded in joining a Late Breaking Clinical Trial Session at a major cardiology congress.
The BRAHMS Aktiengesellschaft conducts researches, develops, produces and markets innovative diagnostic biomarkers. It is one of the three largest biotechnology companies in Germany. The company sells its products in more than 65 countries via its own subsidiary companies and sales organizations as well as laboratory systems from its own production and globally operating licensees. The headquarter of BRAHMS is at Hennigsdorf / Berlin, where about 220 out of 400 of the world wide employees of the company are posted.
4.lactate dehydrogenase
Peak in 72 hours
Lactate dehydrogenase catalyses the conversion of pyruvate to lactate. LDH-1 isozyme is normally found in the heart muscle and LDH-2 is found predominately in blood serum. A high LDH-1 level to LDH-2 suggest MI. LDH levels are also high in tissue breakdown or hemolysis. It can mean cancer, meningitis, encephalitis, or HIV. this usually back to normal 10–14 days.
5.Aspartate transaminase
(AST) This was the first used.It is not specific for heart damage, and it is also one of the liver function tests.
6.Myoglobin.
Rinsing in 2 hours.
Myoglobin is used less than the other markers. Myoglobin is the primary oxygen-carrying pigment of muscle tissue. It is high when muscle tissue is damaged but it lacks specificity. It has the advantage of responding very rapidly, rising and falling earlier than CK-MB or troponin. It also has been used in assessing reperfusion after thrombolysis.
7.Ischemia-modified albumin.
(IMA) low specificity IMA can be detected via the albumin cobalt binding (ACB) test, a limited available FDA approved assay. Myocardial ischemia alters the N-terminus of albumin reducing the ability of cobalt to bind to albumin. IMA measures ischemia in the blood vessels and thus returns results in minutes rather than traditional markers of necrosis that take hours. ACB test has low specificity therefore generating high number of false positives and must be used in conjunction with typical acute approaches such as ECG and physical exam. Additional studies are required.
8.Glycogen phosphorylaseisoenzyme BB
High sensitivity and specificity early after chest pain.Glycogenphosphorylaseisoenzyme BB (abbreviation: GPBB) is an isoenzyme of glycogen phosphorylase. Glycogen phosphorylase exists in 3 isoforms. One of these Isoforms is GP-BB. This isoform exists in heart and brain tissue. Because of the blood-brain barrier GP-BB can be seen as heart muscle specifc. During the process of ischemia, GP-BB is converted into a soluble form and is released into the blood. This isoform of the enzyme exists in cardiac (heart) and brain tissue. GP-BB is one of the “new cardiac markers” which are discussed to improve early diagnosis in acute coronary syndrome. A rapid rise in blood levels can be seen in myocardial infarction and unstable angina. GP-BB elevated 1-3 hours after process of ischemia.
9.Adiponectin.
ADIPONECTIN IS AN adipocyte-derived protein that has gainedconsiderable interest due to its positive effects on insulinsensitivity , atherosclerosis , and inflammation , hereby linking adipose tissue with the cornerstones of themetabolic syndrome.
There is substantial experimental and clinical evidence thatadiponectin protects the vascular endothelium against the processesleading to atherosclerosis. Experimentally, adiponectinknockout animals show an increased neointimal formation aftervascular injury as compared with wild-type littermates ,whereas adiponectin-deficient mice infected with an adenovirusoverexpressing mouse adiponectin showed a normal vascular responseto injury . Furthermore, in the ApoE-deficient mouse, a modelof accelerated atherosclerosis, breeding with adiponectin transgenicmice inhibited the progression of atherosclerosis despite anunaltered glucose and lipid metabolism, suggesting that adiponectinpossessed direct antiatherogenicactions .
In keeping with the experimental support for a vasoprotectiveeffect of adiponectin, several clinical investigations basedon cross-sectional study cohorts have reported on reduced circulatingadiponectin levels in patients with verified coronary heartdisease (CHD). However, some studies have not beenable to demonstrate an association between low levels of adiponectinand an increased risk for CHD , and others have shown thatthe relationship becomes insignificant after adjustment forhigh-density lipoprotein (HDL) cholesterol . On theother hand, nested case control studies have shown that healthysubjects with adiponectin levels within the upper 20% rangehave a 2-fold reduced risk for myocardial infarction anda 7-fold reduced risk for progression of coronary artery calcification. We are not aware of studies describing the relationshipbetween adiponectin and the risk for CHD in population-basedcohorts.
Insulin resistance is a major risk factor for the developmentof atherosclerosis , and it also affects plasma levelsof adiponectin, which become gradually decreased with increasinginsulin resistance . Although adiponectin exerts potentinsulin-sensitizing actions in experimental in vivo models, it remains to be clarified whether the inverse associationbetween adiponectin and insulin sensitivity is a cause-effectrelationship. Thus, it could be speculated that the observedrelationship between adiponectin and the risk for CHD simplyreflects changes in insulin sensitivity. Based on these considerations,we found it of interest to study the risk for CHD and its relationshipwith plasma adiponectin and measures of insulin sensitivityin a population-based cohort of healthy 70-yr-old men followedfor more than 10 yr.
10.Adrenomedullin.
Adrenomedullinis a 52-amino acid peptide originally isolatedfrom pheochromocytoma cells. It has been detected in arange of tissues, including the heart, vasculature, kidney,adrenal medulla, lung, and brain. In experimental heartfailure, adrenomedullin expression is increased and peptidelevels rise, and administered peptide has powerful vasodilatoreffects, increases cardiac output and is natriuretic.Plasma concentrations are in the low picomolar range in healthyindividuals, but they increase in those with hypertension andcongestive heart failure (CHF) in proportion to the severityof the disease. In heart failure, plasma adrenomedullinis inversely related to left ventricular ejection fraction (LVEF)and is positively associated with left ventricular (LV) end-diastolicpressure. At least two reports have indicated that plasmaadrenomedullin levels act as an indicator of prognosis afteracute MI.
There are no published data relating plasma concentrations ofeither N-BNP or adrenomedullin to cardiovascular prognosis inpatients with established ischemic LV dysfunction. We hypothesizedthat plasma levels of either or both peptides would have independentprognostic utility in such patients and also assist in predictingany benefit from treatment with carvedilol. We report the resultsfrom 297 patients with ischemic LV impairment who were randomlyassigned to treatment with carvedilol or placebo for CHF
Kinetics of cardiac markers in myocardial infarction with or without reperfusion treatment.
References
1. The Joint European Society of Cardiology/American College of Cardiology Committee. Myocardial infarction redefined – a consensus document of the Joint European Society of Cardiology/American College of Cardiology Committee for the redefinition of myocardial infarction. J Am CollCardiol 2000;36:959-69.
2. Schroeder JS, Lamb IH, Hu M. Do patients in whom myocardial infarction has been ruled out have a better prognosis after hospitalization than those surviving infarction? N Engl J Med 1980;303:1-5.
3. Hamm CW, Braunwald E. A classification of unstable angina revisited. Circulation 2000;102:118-22.
4. Pennell JP. Optimizing medical management of patients with pre-end-stage renal disease. Am J Med 2001;111:559-68.
5. Chen HH, Burnett JC Jr. The natriuretic peptides in heart failure: diagnostic and therapeutic potentials. ProcAssoc Am Physicians 1999;111:406-16.
6. Ridker PM. High-sensitivity C-reactive protein: potential adjunct for global risk assessment in the primary prevention of cardiovascular disease. Circulation 2001;103:1813-8.
7. Campbell B, Badrick T, Flatman R, Kanowski D. Limited clinical utility of high-sensitivity plasma C-reactive protein assays. Ann ClinBiochem 2002;39:85-8. BRAHMS Aktiengesellschaft
http://www.innovations-report.com/html/reports/life_sciences/cardiac_marker_copeptin_accelerates_diagnosis_acute_135172.html
9.http://en.wikipedia.org/wiki/Reference_ranges_for_blood_tests#Cardiac_tests.for cardiac markers refrencereanges.
10.http://content.onlinejacc.org/cgi/content/full/37/7/1781.foradrenomedullin.
Retrieved from “http://www.articlesbase.com/medicine-articles/cardiac-markers-new-and-old-3698627.html”
(ArticlesBase SC #3698627)
hyder514 -
About the Author:
]]>
Rate this Article
vote(s)
0 vote(s)
Feedback
RSS
Print
Email
Re-Publish
Source: http://www.articlesbase.com/medicine-articles/cardiac-markers-new-and-old-3698627.html
Article Tags:
cardiac markers
Latest Medicine Articles
More from hyder514
Cooling Therapy for Cardiac Arrest
Only 5 percent of people who suffer cardiac arrest survive. Doctors are testing new “icy” treatments to keep the brain and heart safe from damage during cardiac arrest. (01:45)
Recovery from Robotic Cardiac Surgery
Dr. Raczkowski describes the recovery process from robotic cardiac surgery in comparison to the recovery after traditional cardiac surgery. (01:04)
Can Lung Conditions Trigger Cardiac Rhythm Disturbances
Dr. Sanderson discusses if lung conditions can trigger cardiac rhythm disturbances. (00:50)
Cardiac Arrhythmia and Heart Attacks
Learn about the correlation between cardiac arrhythmia and heart attacks. (01:17)
In this video, Dr. Robert O’Connor, discusses how cardiac arrest is treated at the hospital. (01:27)
Studies have shown that many patients with AMI who are eligible for reperfusion therapy do not receive it. Moreover, of those who do receive it, the time to administration of thrombolytic therapy, or “door-to-needle time” is often delayed, jeopardizing myocardium and leading to greater morbidity and mortality.
By:
Pushpa Lathal
Health>
Diseases and Conditionsl
Jul 04, 2009
lViews: 626
Reasons Why Those At Risk Should Take A Cardiac Stress Test
If you have certain medical symptom such as hypertension, diabetes, rapid or irregular heart beats, and so on, your doctor may request that you take a stress test. Normal heart test such as listening through a stethoscope, taking heart beat and blood pressure, etcetera, cannot detect many heart problems – because they’re given while the patient is at rest. Many problems of the heart and circulatory system only reveal themselves when under stress.
By:
Ellen Hustonl
Health>
Wellnessl
Mar 31, 2009
Conditions Cardiac conditions Certain subtypes of troponin (cardiac troponin I and T) are very sensitive and specific indicators of damage to the heart muscle (myocardium)
By:
viedyl
Business>
Public Relationsl
Oct 08, 2010
Reference ranges for blood tests
Interpretation The range is usually defined as the set of values 95 percent of the normal population falls within (that is, 95% prediction interval), or two standard deviations from the mean
By:
dpdpl
Business>
Public Relationsl
May 06, 2010
lViews: 778
Diagnosing Acute Coronary Syndrome In An Accident And Emergency Department
What are acute coronary symptoms and if you have them what should your hospital do to help you?
By:
Nick Jervisl
Lawl
May 17, 2010
Point of Care Analyzers – Recertified
Recertified models of point of care analyzers offer the same level of performance, consistency and accuracy as brand new products.
By:
Jeremy Linderl
Healthl
Jun 15, 2010
Dude, these briefs could save your life
SAN DIEGO – A team of U.S. scientists has designed some new men’s briefs that may be comfortable, durable and even stylish but, unlike most underpants, may be able to save lives.
By:
JerryLool
Health>
Men’s Healthl
Jun 14, 2010
Denosumab Approved for Cancer Patients With Bone Metastases
Bisphosphonates, fosamxa, have already had a huge impact on the natural history of this complication. Denosumab has shown superiority over the bisphosphonate zolendronic acid in 2 of 3 trials that tested the agents head to head in cancer patients with bone metastases. Prolia is much better than bisphosphonate drug used for treatment of osteoporosis
By:
alam.mdl
Health>
Medicinel
Nov 21, 2010
HCG diet-one of the well known method of losing excess fat
HCG diet is one of the well known methods of losing excess fat. HCG is increasingly becoming popular these days as most of the people are trying this and getting benefit. For more you can read the article.
By:
william blakel
Health>
Medicinel
Nov 21, 2010
Cultivate is a medication used for the treatment of inflammation of the skin
By:
Medical Infol
Health>
Medicinel
Nov 21, 2010
Betagan medication is used for reducing the stress in the eye.
By:
Medical Infol
Health>
Medicinel
Nov 21, 2010
Canestan is used for the treatment of fungus infection
By:
Medical Infol
Health>
Medicinel
Nov 21, 2010
Foradil medication is used for relaxing the muscles of the air passage to improve breathing problem.
By:
Medical Infol
Health>
Medicinel
Nov 21, 2010
Gemfibrozil is used for reducing the level of cholesterol and triglycerides
By:
Medical Infol
Health>
Medicinel
Nov 21, 2010
Remedy Migraine Drugs or Just Another Headache?
We have all had garden variety headaches from time to time. Such as sleep, drinking water or aspirin or Tylenol, you can crush these “tension headaches” (as doctors call them) quickly and easily
By:
Agung Prasetyol
Health>
Medicinel
Nov 21, 2010
The use of cardiac troponins in the diagnosis of acute myocardial infarction has changed our understanding of coronary artery disease. Cardiac troponins are slowly released from necrosing myocardium so they are detectable in blood for several days. This prolongs the opportunity for identifying an infarction. Cardiac troponins have therefore significantly reduced the diagnostic role of creatine kinase-MB isoenzyme.confusion can arise because there are different non-standardised laboratory assays
By:
hyder514l
Health>
Medicinel
Nov 19, 2010
Add new Comment
Your Name: *
Your Email:
Comment Body: *
Verification code:*
* Required fields
Submit
Your Articles Here
It’s Free and easy
Sign Up Today
Author Navigation
My Home
Publish Article
View/Edit Articles
View/Edit Q&A
Edit your Account
Manage Authors
Statistics Page
Personal RSS Builder
My Home
Edit your Account
Update Profile
View/Edit Q&A
Publish Article
Author Box
hyder514 has 1 articles online
Articles Categories
All Categories
Advertising
Arts & Entertainment
Automotive
Beauty
Business
Careers
Computers
Education
Finance
Food and Beverage
Health
Hobbies
Home and Family
Home Improvement
Internet
Law
Marketing
News and Society
Relationships
Self Improvement
Shopping
Spirituality
Sports and Fitness
Technology
Travel
Writing
Acne
Allergies
Alternative Medicine
Anti Aging
Cancer
Dental Care
Disabilities
Diseases and Conditions
Hair Loss
Hearing
Medical Tourism
Medicine
Men’s Health
Mental Health
Nutrition
Plastic Surgeries
Quit Smoking
Sleep
Supplements & Vitamins
Vision
Wellness
Women’s Health
]]>
Need Help?
Contact Us
FAQ
Submit Articles
Editorial Guidelines
Blog
Site Links
Recent Articles
Top Authors
Top Articles
Find Articles
Site Map
Webmasters
RSS Builder
RSS
Link to Us
Business Info
Advertising
Use of this web site constitutes acceptance of the Terms Of Use and Privacy Policy | User published content is licensed under a Creative Commons License.
Copyright © 2005-2010 Free Articles by ArticlesBase.com, All rights reserved.
Article from articlesbase.com
[/random]
A few nice increased cardiac output images I found:
Hepatoabdominal compression maneuver
Image by M. Ignacio Monge
Sustained compression over the liver (10 sec), resulted in a sudden increase in arterial pressure (probably due to direct transmission of abdominal pressure to the thorax), following by a drop in pulse pressure and stroke volume / cardiac output. Stroke volume variation (SVV) increase significantly during the maneuver. Cardiac output and stroke volume recover was slower than in CVP/Arterial pressure trace. Hemodynamic monitoring was performed using the FloTrac/Vigileo system (Edwards Lifescience).
Stroke volume / central venous pressure changes during volume expansion (500 mL of saline)
Image by M. Ignacio Monge
Changes in stroke volume went opposite to the central venous pressure. See the right side of the graphic: central venous pressure increased and stroke volume went down. This patient was diagnosed of right ventricle disfunction. This graph illustrates the ventricular interdependence behaviour during right heart failure.
FRANK-STARLING test
Image by M. Ignacio Monge
A Frank-Starling principle recreation from a non-preload responder patient. There was no significant increase on stroke volume instead the CVP rised from 15 to 19 mmHg. A regression line was drawn to show the Frank-Starling curve.
increased cardiac output
| Print article | This entry was posted by HealthyB on November 22, 2010 at 3:23 pm, and is filed under Aerobics Cardio. Follow any responses to this post through RSS 2.0. You can leave a response or trackback from your own site. |
about 1 year ago
Since more than 200 persons have visited this graph, I would like that someone make any comments about it.