Right heart failure laboratory findings: Difference between revisions
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{{Right heart failure}} | {{Right heart failure}} | ||
{{CMG}}; {{AE}} [[User:Jad Z Al Danaf|Jad Z Al Danaf]]; [[User:Rim Halaby|Rim Halaby]] | |||
{{CMG}}; [[User:Jad Z Al Danaf|Jad Z Al Danaf]]; [[User:Rim Halaby|Rim Halaby]] | |||
==Overview== | ==Overview== | ||
Laboratory tests are useless in the diagnosis of | Laboratory tests are useless in the diagnosis of heart failure, however they are essential in identifying possible precipitating factors of decompensation, assessing severity of the heart failure, monitoring the side effects of medical treatment and some serve as prognostic markers.<ref>Tago WH, Francis GS, Morrow DA, et al. National Academy of Clinical Biochemistry Laboratory Medicine. National Academy of Clinical Biochemistry Laboratory Medicine practice guidelines: Clinical utilization of cardiac biomarker testing in heart failure. Circulation. 2007; 116:e90-e109.</ref> | ||
In addition, in patients with right | In addition, in patients with right heart failure, an [[arterial blood gas]] can be useful in assessing the degree of [[hypoxemia]]. This can in turn be used to guide therapy with [[oxygen]]. | ||
==Laboratory | ==Laboratory Findings== | ||
====Complete Blood | ====Complete Blood Count (CBC)<ref name="Van">Van der Meer P. and Van Veldhuisen DJ. Anaemia and renal dysfunction in chronic heart failure. Heart. 2009; 95: 1808-1812.</ref>==== | ||
*[[Anemia]] might trigger decompensation of | *[[Anemia]] might trigger decompensation of heart failure. | ||
*Low lymphocyte | *Low [[lymphocyte]] >7000/µL basal [[white blood cell count]] and [[ESR]] >15mm in first hour might indicate worse prognosis | ||
*CBC is to be repeated every 6 months unless needed to be repeated more frequently. | *[[CBC]] is to be repeated every 6 months unless needed to be repeated more frequently. | ||
====Serum Electrolytes and Creatinine<ref name="Van">Van der Meer P. and Van Veldhuisen DJ. Anaemia and renal dysfunction in chronic heart failure. Heart. 2009; 95: 1808-1812.</ref>==== | ====Serum Electrolytes and Creatinine<ref name="Van">Van der Meer P. and Van Veldhuisen DJ. Anaemia and renal dysfunction in chronic heart failure. Heart. 2009; 95: 1808-1812.</ref>==== | ||
*Hypernatremia, increase in serum creatinine and hypokalemia might result from aggressive [[diuretic]] therapy. | *[[Hypernatremia]], increase in [[serum creatinine]] and [[hypokalemia]] might result from aggressive [[diuretic]] therapy. | ||
*Hypokalemia and hypomagnesemia as side effects of potassium-losing diuretics | *[[Hypokalemia]] and [[hypomagnesemia]] as side effects of potassium-losing diuretics. | ||
*Hyperkalemia secondary to renal failure, excessive potassium intake or as a side effect of diuretics (ACR-I, ARB and spironolactone) | *[[Hyperkalemia]] secondary to [[renal failure]], excessive [[potassium]] intake or as a side effect of [[diuretics]] (ACR-I, [[ARB]] and [[spironolactone]]) | ||
*Target range for K+ should be 4-5 mEq/L | *Target range for K+ should be 4-5 mEq/L | ||
*To be repeated daily to adjust dose of diuretics and then every 2-3 months in stable patients. | *To be repeated daily to adjust dose of [[diuretics]] and then every 2-3 months in stable patients. | ||
====Serum Uric Acid==== | ====Serum Uric Acid==== | ||
*Hyperuricemia can be seen in [[renal failure]] and secondary to [[thiazide]] diuretic use. It is also seen in | *[[Hyperuricemia]] can be seen in [[renal failure]] and secondary to [[thiazide]] diuretic use. It is also seen in [[cachexia|cachectic]] patients. | ||
*It is to be repeated every 6 months in stable patients and 3 months in patients on high [[diuretic]] doses. | *It is to be repeated every 6 months in stable patients and 3 months in patients on high [[diuretic]] doses. | ||
====Liver Function Tests==== | ====Liver Function Tests==== | ||
*Elevated | *Elevated [[alkaline phosphatase]], liver [[transaminases]] and total [[bilirubin]] can be secondary to [[liver]] congestion. | ||
*Elevated gamma | *Elevated [[gamma glutamyl transferase]] values are sensitive but nonspecific indicators of [[heart failure]]. | ||
* | *[[Hypoalbuminemia]] can be seen in malnutrition or renal dysfunction. It also raises the suspicion of [[protein losing enteropathy]] which necessitates checking stool [[alpha 1-antitrypsin]]. | ||
*It is to be repeated every 6-12 months in stable patients, during every | *It is to be repeated every 6-12 months in stable patients, during every heart failure decompensatory episode and in pathological [[weight loss]]. | ||
====Coagulation Tests==== | ====Coagulation Tests==== | ||
*INR especially during anticoagulant therapy or in setting of hepatic dysfunction-nutmeg liver must be measured. | *[[INR]] especially during anticoagulant therapy or in setting of hepatic dysfunction-nutmeg liver must be measured. | ||
====Cardiac Troponins==== | ====Cardiac Troponins==== | ||
*Highly sensitive troponin I (hs-cTnI) serves as outcome predictors with more sensitivity then cardiac | *Highly sensitive [[troponin I]] (hs-cTnI) serves as outcome predictors with more sensitivity then cardiac [[troponin T]] (cTnT). | ||
====Thyroid Hormones==== | ====Thyroid Hormones==== | ||
*[[Thyroid]] hormones must be measured in cases of [[atrial fibrillation]], dilated [[cardiomyopathy]], patient on [[amiodarone]] therapy and in patients older than 65 years of age. | *[[Thyroid]] hormones must be measured in cases of [[atrial fibrillation]], dilated [[cardiomyopathy]], patient on [[amiodarone]] therapy and in patients older than 65 years of age. | ||
*Blood glucose level in non-diabetics | *[[Blood glucose]] level in non-diabetics | ||
*High | *High blood glucose level in non-diabetic patients can be secondarily to high diuretic doses such as [[thiazides]]. | ||
====Neurohormonal Prognostic Markers==== | ====Neurohormonal Prognostic Markers==== | ||
*B-type natriuretic peptide and NT-proBNP | *[[B-type natriuretic peptide]] ([[BNP]]) and NT-proBNP | ||
*Endothelin-1 | *[[Endothelin-1]] | ||
*Miscellaneous (Plasma | *Miscellaneous (Plasma [[renin]] activity, [[ANP]], NE, hsCRP, calitonin gene related peptide, [[prostaglandins]], [[erythropoietin]])<ref>Haddad F. et al. Right Ventricular function in Cardiovascular Disease, Part II: Pathophysiology, Clinical Importance and Management of Right Ventricular failure. Circulation. 2008;117:1717-1731</ref><ref>Maeder M, Fehr T, Rickli H, Ammann P. Sepsis-associated myocardial dysfunction: diagnostic and prognostic impact of cardiac troponins and natriuretic peptides. Chest. 2006;129:1349 –1366.</ref><ref>Pousset F, Isnard R, Lecnat R et al. Prognostic value of plasma endothelin-1 in patients with chroninc heart failure. Eur Heart J. 1997; 18:254-258.</ref><ref>Hobbs RE. Using BNP to diagnose, manage, and treat heart failure. Cleve Clin J Med 2003;70:333–6.</ref> | ||
Shown below is a table summarizing the interpretation of the levels of [[BNP]] and NT-proBNP levels. | |||
{| | {|class="wikitable" border="1" | ||
|- | |- | ||
|'''BNP''' | |'''BNP''' | ||
Line 59: | Line 58: | ||
|- | |- | ||
|>500 pg/mL | |>500 pg/mL | ||
>900 pg/mL (50-75 years old) | |>900 pg/mL (50-75 years old) | ||
|Likely decompensated | |Likely decompensated heart failure | ||
|- | |- | ||
| | | | ||
|>1,800 pg/mL (>75 years old) | |>1,800 pg/mL (>75 years old) | ||
|Likely decompensated heart failure | |Likely decompensated heart failure | ||
|} | |} | ||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
{{WH}} | |||
{{WS}} | |||
[[Category:Disease]] | |||
[[Category:Cardiology]] | [[Category:Cardiology]] | ||
[[Category:Pulmonology]] | [[Category:Pulmonology]] | ||
[[Category: | [[Category:Up-To-Date]] | ||
[[Category: | [[Category:Up-To-Date cardiology]] | ||
Latest revision as of 00:02, 30 July 2020
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Jad Z Al Danaf; Rim Halaby
Overview
Laboratory tests are useless in the diagnosis of heart failure, however they are essential in identifying possible precipitating factors of decompensation, assessing severity of the heart failure, monitoring the side effects of medical treatment and some serve as prognostic markers.[1] In addition, in patients with right heart failure, an arterial blood gas can be useful in assessing the degree of hypoxemia. This can in turn be used to guide therapy with oxygen.
Laboratory Findings
Complete Blood Count (CBC)[2]
- Anemia might trigger decompensation of heart failure.
- Low lymphocyte >7000/µL basal white blood cell count and ESR >15mm in first hour might indicate worse prognosis
- CBC is to be repeated every 6 months unless needed to be repeated more frequently.
Serum Electrolytes and Creatinine[2]
- Hypernatremia, increase in serum creatinine and hypokalemia might result from aggressive diuretic therapy.
- Hypokalemia and hypomagnesemia as side effects of potassium-losing diuretics.
- Hyperkalemia secondary to renal failure, excessive potassium intake or as a side effect of diuretics (ACR-I, ARB and spironolactone)
- Target range for K+ should be 4-5 mEq/L
- To be repeated daily to adjust dose of diuretics and then every 2-3 months in stable patients.
Serum Uric Acid
- Hyperuricemia can be seen in renal failure and secondary to thiazide diuretic use. It is also seen in cachectic patients.
- It is to be repeated every 6 months in stable patients and 3 months in patients on high diuretic doses.
Liver Function Tests
- Elevated alkaline phosphatase, liver transaminases and total bilirubin can be secondary to liver congestion.
- Elevated gamma glutamyl transferase values are sensitive but nonspecific indicators of heart failure.
- Hypoalbuminemia can be seen in malnutrition or renal dysfunction. It also raises the suspicion of protein losing enteropathy which necessitates checking stool alpha 1-antitrypsin.
- It is to be repeated every 6-12 months in stable patients, during every heart failure decompensatory episode and in pathological weight loss.
Coagulation Tests
- INR especially during anticoagulant therapy or in setting of hepatic dysfunction-nutmeg liver must be measured.
Cardiac Troponins
- Highly sensitive troponin I (hs-cTnI) serves as outcome predictors with more sensitivity then cardiac troponin T (cTnT).
Thyroid Hormones
- Thyroid hormones must be measured in cases of atrial fibrillation, dilated cardiomyopathy, patient on amiodarone therapy and in patients older than 65 years of age.
- Blood glucose level in non-diabetics
- High blood glucose level in non-diabetic patients can be secondarily to high diuretic doses such as thiazides.
Neurohormonal Prognostic Markers
- B-type natriuretic peptide (BNP) and NT-proBNP
- Endothelin-1
- Miscellaneous (Plasma renin activity, ANP, NE, hsCRP, calitonin gene related peptide, prostaglandins, erythropoietin)[3][4][5][6]
Shown below is a table summarizing the interpretation of the levels of BNP and NT-proBNP levels.
BNP | NT-proBNP | Comment |
<100 pg/mL | <300 pg/mL | Unlikely decompensated heart failure |
>500 pg/mL | >900 pg/mL (50-75 years old) | Likely decompensated heart failure |
>1,800 pg/mL (>75 years old) | Likely decompensated heart failure |
References
- ↑ Tago WH, Francis GS, Morrow DA, et al. National Academy of Clinical Biochemistry Laboratory Medicine. National Academy of Clinical Biochemistry Laboratory Medicine practice guidelines: Clinical utilization of cardiac biomarker testing in heart failure. Circulation. 2007; 116:e90-e109.
- ↑ 2.0 2.1 Van der Meer P. and Van Veldhuisen DJ. Anaemia and renal dysfunction in chronic heart failure. Heart. 2009; 95: 1808-1812.
- ↑ Haddad F. et al. Right Ventricular function in Cardiovascular Disease, Part II: Pathophysiology, Clinical Importance and Management of Right Ventricular failure. Circulation. 2008;117:1717-1731
- ↑ Maeder M, Fehr T, Rickli H, Ammann P. Sepsis-associated myocardial dysfunction: diagnostic and prognostic impact of cardiac troponins and natriuretic peptides. Chest. 2006;129:1349 –1366.
- ↑ Pousset F, Isnard R, Lecnat R et al. Prognostic value of plasma endothelin-1 in patients with chroninc heart failure. Eur Heart J. 1997; 18:254-258.
- ↑ Hobbs RE. Using BNP to diagnose, manage, and treat heart failure. Cleve Clin J Med 2003;70:333–6.