Category: Critical Care Nursing Many experts are skeptical about the clinical utility of static pressures for guiding hemodynamic management. Neither CVP nor PAOP is a good predictor of preload responsiveness (i.e., an increase in CO or SV after fluid bolus administration).
Category: Critical Care Nursing As the management of the critically ill patient has evolved, the question of volume (i.e., preload) responsiveness has taken priority over static parameters like central venous pressure (CVP) and pulmonary artery occlusion pressure (PAOP).
Category: Critical Care Nursing Echocardiography is a valuable tool to identify the etiology of hemodynamic instability and to guide clinical management in a critical care setting. One small study showed it use was associated with improved intensive care unit survival.
Category: Critical Care Nursing BNP remains a good indicator of ventricular dysfunction and myocardial wall stress, but which cutoff levels should be used and what the clinician should do when the BNP exceeds those levels remain unclear.
Category: Critical Care Nursing Women and older individuals traditionally have higher BNP levels, and so age- and gender-specific cutoffs may be needed. Whereas obese individuals have lower values, renal dysfunction increases BNP serum levels, sometimes dramatically.
Category: Critical Care Nursing ProBNP is released by the heart in response to stretching of the wall and after ischemia. Subsequently, it is cleaved into active B-type natriuretic peptide (BNP) and N-terminal pro-BNP (NT-proBNP), both of which can be measured in blood.
Category: Critical Care Nursing Cardiac myosin-binding protein C (cMyC) rises more rapidly in the systemic circulation than high-sensitivity cardiac troponin T (hs-cTnT), perhaps as a result of its higher myocardial concentration.
Category: Critical Care Nursing Cardiac myosin-binding protein C (cMyC) is a cardiac-restricted protein that enters the systemic circulation after myocardial injury, is more abundant than troponin and has been recently identified as a new candidate biomarker of cardiac injury.
Category: Critical Care Nursing Regardless of the cause, it is clear that elevation of serum troponin levels is associated with a worsened outcome both in and out of the intensive care unit, even after adjustment for severity of the disease.
Category: Critical Care Nursing Although detectable troponin levels usually emanate from myocardial cells, they may not always represent irreversible cell death or myocardial ischemia. Renal dysfunction is another factor associated with elevated troponin levels.
Category: Critical Care Nursing Troponin release in the critically ill may not always represent myocardial cell death. Endotoxin, cytokines and inflammatory mediators, along with catecholamines and conditions such as hypotension or hypoxia, may cause the breakdown of troponin.
Category: Critical Care Nursing Demand ischemia (type 2 MI) can also lead to troponin release. Other causes of elevated troponin include sustained brady-/tachy-arrhythmias, hypotension, shock, cardiomyopathy, sepsis, pulmonary embolism and strenuous exercise.
Category: Critical Care Nursing The challenge for the clinician, and particularly for the intensivist, is that although the elevation of serum troponin is highly specific for myocardial cell damage, not all of the damage is a consequence of the rupture of an atherosclerotic plaque.
Category: Critical Care Nursing Troponin elevations are sensitive and specific for myocardial cellular injury. False positives because of fibrin interference or antibodies are infrequent. Even minor increases in troponin values correlate with adverse outcomes in NSTE-ACS.
Category: Critical Care Nursing Creatine kinase (CK) and its isoenzyme MB (CK-MB) were the initial biomarkers of choice for myocardial injury and infarction in the 1970s, but were later superseded by troponin T and I, because of their increased sensitivity and specificity.
