Cardiogenic shock laboratory findings: Difference between revisions
Joao Silva (talk | contribs) |
|||
| (18 intermediate revisions by 2 users not shown) | |||
| Line 1: | Line 1: | ||
__NOTOC__ | __NOTOC__ | ||
{{Cardiogenic shock}} | {{Cardiogenic shock}} | ||
{{CMG}}; {{AE}} {{JS}} | {{CMG}}; {{AE}} {{JS}} {{sali}} | ||
==Overview== | ==Overview== | ||
[[Biomarkers]] of [[cardiac]] [[myonecrosis]] are useful to gauge the severity of acute underlying [[myocardial injury]] in conditions such as [[fulminant]] [[myocarditis]]. In [[ACS]], [[cardiac]] [[troponin]] is noted to be elevated and has a rise-and-fall pattern consistent with [[acute ischemic injury]]. A mismatch between the degree of segmental dysfunction on imaging and [[troponin]] release may be noted in the setting of [[stunned]]/[[hibernating]] [[myocardium]] or when presentation is significantly delayed after the [[ischemic]] insult. [[Myocardial]] [[necrosis]] [[biomarker]] levels may provide an idea of the extent of [[myocardial]] injury, whereas serial measurements are useful in assessing early washout after successful [[reperfusion]] and in estimating the amount of [[cardiac]] [[necrosis]]. [[Natriuretic]] [[peptides]] are significantly elevated in the setting of acute [[HF]] culminating in CS and are associated with [[mortality]] in [[MI]]-associated CS. [[Oxygen-carrying capacity]] is the product of [[cardiac output]] and the [[oxygen]] content of [[blood]]. Thus, an ineffective CI will result in inadequate peripheral tissue oxygen delivery. Elevated arterial lactic acid levels are nonspecifically indicative of tissue hypoxia but are associated with mortality in CS.The pathogenesis of [[lactate]] production in CS is uncertain, although [[impaired oxygen]] delivery, [[stress-induced hyperlactatemia]], and impaired clearance are likely contributors. A peripheral oxygen demand-delivery mismatch will result in low central venous oxygen measurements. A mixed venous oxygen saturation sample is ideally obtained from the distal port of a [[pulmonary artery catheter]] ([[PAC]]) and is a reflection of [[oxygen]] saturation from blood returning to the [[heart]] via the [[superior]] and [[inferior vena cava]], as well as the [[coronary]] [[sinus]]. Serial measurements of [[arterial]] [[lactate]] and mixed [[venous]] [[oxygen]] saturation levels may be helpful to temporally monitor responses to therapeutic interventions. [[Arterial blood gas]] measurements also permit the assessment of [[arterial] [[oxygenation]] and [[ventilation]], as well as [[metabolic]] and [[respiratory]] [[acid-base]] disorders. [[Acute kidney injury]], which is reflected by a rise in serum creatinine and a potential reduction in urinary output, in the setting of CS may indicate renal hypoperfusion and is associated with poor outcomes. It should be noted that novel [[renal biomarkers]] such as [[neutrophil]] [[gelatinase–associated lipocalcin]], [[kidney injury]] molecule 1, and cystatin C were not more effective than standard evaluation with serum creatinine for assessing risk. Acute ischemic or congestive liver injury can occur in the setting of CS and manifests as a marked [[elevation]] in serum [[aspartate aminotransferase]], [[alanine aminotransferase]], serum [[bilirubin]], and [[lactate dehydrogenase]] levels, often accompanied by an increase in [[prothrombin time]] with a peak at 24 to 72 hours that subsequently recovers to baseline within 5 to 10 days, and a ratio of [[alanine aminotransferase]] to [[lactate dehydrogenase]] of <1.5. This should be differentiated from chronic to subacute elevation of [[liver function abnormalities]] in the setting of [[venous congestion]] resulting from right-sided HF. | |||
==Laboratory Findings== | ==Laboratory Findings== | ||
''As in all laboratory tests, these must be ordered in order to confirm, sustain or rule out a clinical [[diagnosis]] that has been reached after proper [[Medical history|history]] and [[physical examination]] have been made. In the case of cardiogenic shock, these may include:''<ref>{{Cite book | last1 = Longo | first1 = Dan L. (Dan Louis) | title = Harrison's principles of internal medici | date = 2012 | publisher = McGraw-Hill | location = New York | isbn = 978-0-07-174889-6 | pages = }}</ref> | ''As in all laboratory tests, these must be ordered in order to confirm, sustain or rule out a clinical [[diagnosis]] that has been reached after proper [[Medical history|history]] and [[physical examination]] have been made. In the case of cardiogenic shock, these may include:''<ref>{{Cite book | last1 = Longo | first1 = Dan L. (Dan Louis) | title = Harrison's principles of internal medici | date = 2012 | publisher = McGraw-Hill | location = New York | isbn = 978-0-07-174889-6 | pages = }}</ref><ref>{{cite book | last = Parrillo | first = Joseph | title = Critical care medicine principles of diagnosis and management in the adult | publisher = Elsevier/Saunders | location = Philadelphia, PA | year = 2013 | isbn = 0323089291 }}</ref> | ||
===Arterial Blood Gas=== | ===Arterial Blood Gas=== | ||
| Line 13: | Line 13: | ||
*[[Metabolic acidosis]], possibly compensated by [[respiratory alkalosis]] | *[[Metabolic acidosis]], possibly compensated by [[respiratory alkalosis]] | ||
===Markers | ===Cardiac Markers=== | ||
*Elevated [[cardiac markers]], such as: | *Elevated [[cardiac markers]], such as: | ||
:*[[Troponin I]] and [[Troponin T]] | :*[[Troponin I]] and [[Troponin T]] | ||
| Line 19: | Line 19: | ||
===Complete Blood Count=== | ===Complete Blood Count=== | ||
*Elevated [[white blood cell count]] ([[WBC]]), typically with a left shift. | *Elevated [[white blood cell count]] ([[WBC]]), typically with a left shift. It should be noted that the [[WBC]] may be elevated in [[STEMI]] and [[shock]] in general, due to demargination of [[neutrophils]]. | ||
*[[Leukopenia]] may be present later in [[shock]] or in alternate diagnosis of sepsis | |||
*[[Platelet count]] may be elevated in early stages of [[shock]] due to the stress caused by this condition, however, [[thrombocytopenia]] may be noted later, in situations of resuscitation from massive [[hemorrhage]], or in alternate [[diagnosis]] of [[sepsis]]. | |||
===Renal Function=== | ===Renal Function=== | ||
| Line 33: | Line 34: | ||
===Serum Lactate=== | ===Serum Lactate=== | ||
*[[Lactic acidosis]] ([[Anion Gap Acidosis]]). | *[[Lactic acidosis]] ([[Anion Gap Acidosis]]). The level of [[lactic acid]], particularly its serial determinations, along with compensatory decrease in [[serum bicarbonate]], are markers of the extent of [[hypoperfusion]] and valuable in gauging a patient's [[prognosis]]. However, its utility is limited by the fact that [[lactic acid]] rises later in [[tissue]] [[hypoperfusion]] therefore, by the time it is elevated, severe tissue [[ischemia]] will already have occurred. This downside is aggravated by the constant clearance of [[lactic acid]] by the [[liver]] in the presence of normal [[hepatic]] function.<ref name="pmid1758176">{{cite journal| author=Cilley RE, Scharenberg AM, Bongiorno PF, Guire KE, Bartlett RH| title=Low oxygen delivery produced by anemia, hypoxia, and low cardiac output. | journal=J Surg Res | year= 1991 | volume= 51 | issue= 5 | pages= 425-33 | pmid=1758176 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1758176 }} </ref> | ||
==References== | ==References== | ||
Latest revision as of 18:13, 8 January 2020
|
Cardiogenic Shock Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Cardiogenic shock laboratory findings On the Web |
|
American Roentgen Ray Society Images of Cardiogenic shock laboratory findings |
|
Risk calculators and risk factors for Cardiogenic shock laboratory findings |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2] Syed Musadiq Ali M.B.B.S.[3]
Overview
Biomarkers of cardiac myonecrosis are useful to gauge the severity of acute underlying myocardial injury in conditions such as fulminant myocarditis. In ACS, cardiac troponin is noted to be elevated and has a rise-and-fall pattern consistent with acute ischemic injury. A mismatch between the degree of segmental dysfunction on imaging and troponin release may be noted in the setting of stunned/hibernating myocardium or when presentation is significantly delayed after the ischemic insult. Myocardial necrosis biomarker levels may provide an idea of the extent of myocardial injury, whereas serial measurements are useful in assessing early washout after successful reperfusion and in estimating the amount of cardiac necrosis. Natriuretic peptides are significantly elevated in the setting of acute HF culminating in CS and are associated with mortality in MI-associated CS. Oxygen-carrying capacity is the product of cardiac output and the oxygen content of blood. Thus, an ineffective CI will result in inadequate peripheral tissue oxygen delivery. Elevated arterial lactic acid levels are nonspecifically indicative of tissue hypoxia but are associated with mortality in CS.The pathogenesis of lactate production in CS is uncertain, although impaired oxygen delivery, stress-induced hyperlactatemia, and impaired clearance are likely contributors. A peripheral oxygen demand-delivery mismatch will result in low central venous oxygen measurements. A mixed venous oxygen saturation sample is ideally obtained from the distal port of a pulmonary artery catheter (PAC) and is a reflection of oxygen saturation from blood returning to the heart via the superior and inferior vena cava, as well as the coronary sinus. Serial measurements of arterial lactate and mixed venous oxygen saturation levels may be helpful to temporally monitor responses to therapeutic interventions. Arterial blood gas measurements also permit the assessment of [[arterial] oxygenation and ventilation, as well as metabolic and respiratory acid-base disorders. Acute kidney injury, which is reflected by a rise in serum creatinine and a potential reduction in urinary output, in the setting of CS may indicate renal hypoperfusion and is associated with poor outcomes. It should be noted that novel renal biomarkers such as neutrophil gelatinase–associated lipocalcin, kidney injury molecule 1, and cystatin C were not more effective than standard evaluation with serum creatinine for assessing risk. Acute ischemic or congestive liver injury can occur in the setting of CS and manifests as a marked elevation in serum aspartate aminotransferase, alanine aminotransferase, serum bilirubin, and lactate dehydrogenase levels, often accompanied by an increase in prothrombin time with a peak at 24 to 72 hours that subsequently recovers to baseline within 5 to 10 days, and a ratio of alanine aminotransferase to lactate dehydrogenase of <1.5. This should be differentiated from chronic to subacute elevation of liver function abnormalities in the setting of venous congestion resulting from right-sided HF.
Laboratory Findings
As in all laboratory tests, these must be ordered in order to confirm, sustain or rule out a clinical diagnosis that has been reached after proper history and physical examination have been made. In the case of cardiogenic shock, these may include:[1][2]
Arterial Blood Gas
- Hypoxemia
- Metabolic acidosis, possibly compensated by respiratory alkalosis
Cardiac Markers
- Elevated cardiac markers, such as:
- Troponin I and Troponin T
- Elevated CK MB
Complete Blood Count
- Elevated white blood cell count (WBC), typically with a left shift. It should be noted that the WBC may be elevated in STEMI and shock in general, due to demargination of neutrophils.
- Leukopenia may be present later in shock or in alternate diagnosis of sepsis
- Platelet count may be elevated in early stages of shock due to the stress caused by this condition, however, thrombocytopenia may be noted later, in situations of resuscitation from massive hemorrhage, or in alternate diagnosis of sepsis.
Renal Function
- Elevated blood urea nitrogen
- Elevated creatinine
In case of prior normal renal function, BUN and creatinine will only be elevated later on the course of the disease. If there is prior renal insufficiency, these values will be elevated earlier.
Hypophosphatemia should be excluded as an underlying cause. Myonecrosis following hypophosphatemia may be observed in refeeding syndrome, as phosphate is used to convert glucose to glycogen.
Liver Function
- Elevated hepatic transaminases, following liver hypoperfusion
Serum Lactate
- Lactic acidosis (Anion Gap Acidosis). The level of lactic acid, particularly its serial determinations, along with compensatory decrease in serum bicarbonate, are markers of the extent of hypoperfusion and valuable in gauging a patient's prognosis. However, its utility is limited by the fact that lactic acid rises later in tissue hypoperfusion therefore, by the time it is elevated, severe tissue ischemia will already have occurred. This downside is aggravated by the constant clearance of lactic acid by the liver in the presence of normal hepatic function.[3]
References
- ↑ Longo, Dan L. (Dan Louis) (2012). Harrison's principles of internal medici. New York: McGraw-Hill. ISBN 978-0-07-174889-6.
- ↑ Parrillo, Joseph (2013). Critical care medicine principles of diagnosis and management in the adult. Philadelphia, PA: Elsevier/Saunders. ISBN 0323089291.
- ↑ Cilley RE, Scharenberg AM, Bongiorno PF, Guire KE, Bartlett RH (1991). "Low oxygen delivery produced by anemia, hypoxia, and low cardiac output". J Surg Res. 51 (5): 425–33. PMID 1758176.