Transcript Cardio LABS

Cardiovascular
Laboratory Medicine
Brenda Beckett, PA-C
Specimen Collection

Fasting
– nothing to eat or drink for 10-12 hours
– can have H2O and medication
Specific Tests to System
- Screening tests: Lipids, CRP,
Homocysteine
- Identifying disease: BNP, cardiac
enzymes
CV Screening Tests-Lipids
FASTING SPECIMEN
 Total Cholesterol
 HDL
 Triglycerides
 LDL - calculated or direct
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Newest Guidelines

Third Report of the National
Cholesterol Education Program
(NCEP) Expert Panel on Detection,
Evaluation, and Treatment of High
Blood Cholesterol in Adults (Adult
Treatment Panel III), or ATP III
Screening
Can screen with Total Cholesterol, if
>200, perform complete lipid profile
 Screening should be performed on
adults every 5 years
 Normal Ranges are not determined as
other lab tests - national standard

Total Cholesterol Levels

< 200 mg/dl

200-239 mg/dl

>= 240 mg/dl

Desirable, low risk for
heart disease

Borderline high

High Cholesterol. In this
range, a person has
twice the risk of heart
disease as person with
<200 mg/dl
HDL-Cholesterol Levels

< 40 mg/dl

40-59 mg/dl

>=60 mg/dl

A major risk factor
for heart disease
 The higher the HDL,
the better
 Considered
protective against
heart disease
LDL-Cholesterol Levels

< 100 mg/dl

Optimal

100-129 mg/dl

Near Optimal/ Above
Optimal
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130-159 mg/dl

Borderline High
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160-189 mg/dl
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High
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>=190 mg/dl

Very High
LDL-Cholesterol Levels

Target levels of LDL are adjusted if
someone has existing risk factors for
cardiovascular disease.

Tables, p 118 Wallach
Triglyceride Levels

< 150 mg/dl

Normal
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150-199 mg/dl

Borderline High
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200-499 mg/dl
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High
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>=500 mg/dl
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Very high
Determining CV Risk


Identify presence of clinical
atherosclerotic disease that confers
high risk for coronary heart disease
(CHD) events (CHD risk equivalent):
• Clinical CHD
• Symptomatic carotid artery disease
• Peripheral arterial disease
• Abdominal aortic aneurysm
Note: Diabetes is regarded as a CHD risk equivalent.
Determining CV Risk, cont

Determine presence of major risk factors
(other than LDL):
• Cigarette smoking
• Hypertension (BP 140/90 mmHg or on antihypertensive
medication)
• Low HDL cholesterol (<40 mg/dl)* HDL >60 counts as a
"negative" risk factor and removes one risk factor from count.
• Family history of premature CHD (CHD in male first
degree relative <55 years; CHD in female first degree
relative <65 years)
• Age (men 45 years; women 55 years)
Determining CV Risk, cont

Determine risk category:
• Establish LDL goal of therapy
• Determine need for therapeutic lifestyle
changes (TLC)
• Determine level for drug consideration
Determining CV Risk, cont

LDL Cholesterol Goals for TLC and
Drug Therapy in Risk Categories:

CHD risk equivalent
<100 mg/dl

2+ risks
<130 mg/dl

0-1 risk
<160 mg/dl
Determining CV Risk, cont

Initiate therapeutic lifestyle changes
(TLC) if LDL is above goal.
– Diet, weight management, physical activity.

Consider adding drug therapy if LDL
continues to exceed goal.

http://www.nhlbi.nih.gov/guidelines/chol
esterol/atglance.htm
Other Screening Tests

Homocysteine
 Amino acid in the blood.
 Increased homocysteine related to increased
risk of coronary heart disease, stroke and
peripheral vascular disease.
 Strongly influenced by diet - folic acid and
vitamins B6 and B12 as well as by genetic
factors
Other Screening Tests
CRP (Cardio or ultrasensitive)
 Traditionally used to diagnose and
monitor acute inflammatory states
 Mild CRP elevation (within the normal,
non-acute-phase range) has recently
emerged as a valuable marker of
cardiovascular risk.
 Measured twice, 2 weeks apart.
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Diagnosis of AMI

A number of laboratory tests are available.

None is completely sensitive and specific for
MI, particularly in the hours following onset of
symptoms.

Timing is important, as are correlation with
patient symptoms, ECGs, and angiographic
studies.
Diagnosis of AMI
CK, Total (Creatine Kinase): Simple,
quick test. Not specific for MI. Three
fractions: MM (skeletal muscle), MB
(cardiac muscle), BB (brain tissue).
 CKMB: Specific for cardiac injury. Rises
2-8 hrs after injury, returns to normal in
2-3 days. Serial testing every 4 hrs can
provide a pattern.

Diagnosis of AMI
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CKMB isoforms:
– 1 and 2. Performed by electrophoresis.
– Ratio of 2 to 1 can determine early cardiac
injury.
– Labor intensive and not routinely used.
Diagnosis of AMI
Troponins I and T: Structural
components of cardiac muscle.
Released with injury. More specific than
CKMB.
 Rise within 3-12 hours, remain elevated
for up to 2 weeks. Difficult to diagnose
reinfarction, helpful with old MI.

Diagnosis of AMI
Myoglobin: Protein in skeletal and
cardiac muscle. Sensitive but not
specific. Rises early
 LDH: Not used routinely. Need to
measure isoenzymes.

On the horizon
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h-FABP: Heart Fatty-Acid Binding Protein

Early detection (as early as 20 min)
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Small cytosolic protein abundant in the heart
 Detects MI and reperfusion
 Renal clearance in few hours
Diagnosis of AMI - ACC
guidelines

Typical rise and fall of biochemical
markers (CKMB and Troponin) and at
least one of the following:
– Ischemic symptoms
– New pathological Q waves on ECG
– Ischemic ECG changes (ST elevation or
depression)
– Coronary artery intervention
Case Study #1
30 yo male, admitted with CC of severe
squeezing pain, lasted 10 min. Began
after dinner. Radiated to L shoulder and
jaw, assoc with palpitations, SOB.
Similar episode 1 mo ago. Smokes
2ppd cigarettes.
 FH: grandfather, father, sister all died
from heart attacks at early age.

Case Study #1
PE: Pale, restless young man in severe
distress due to 8/10 chest pain. Pain
subsided after given nitro. BP 140/85,
HR 90, RR 17, T 98F. Physical exam
unremarkable.
 ECG: Elevated ST segments in
precordial leads.
 Differential Diagnosis?

Case Study #1
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What labs to order to confirm
diagnosis?
Case Study #1

What further testing do you want to
order?
Case Study #1
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Diagnosis?:
CHF

BNP -B-type (brain) natriuretic peptide
 Useful for diagnosing CHF, predicting
morbidity and mortality, and maximizing
therapy in these patients
 First isolated from brain tissue, but is
synthesized primarily in the ventricles of the
heart.
 NT-proBNP (isomer of BNP) testing has the
same clinical utility as BNP
BNP
Increases glomerular filtration rate
 Decreases sodium retention, and
inhibits renin and aldosterone secretion.
 Marker of cardiac dysfunction that
correlates with the severity of
symptomatic and asymptomatic left
ventricular hypertrophy and CHF

CHF
Other laboratory findings in CHF:
 Anemia
 Renal function tests: may have prerenal
azotemia
 Lytes: hypokalemia, hyperkalemia,
hyponatremia

Bacterial Endocarditis
Blood culture: Proper collection, multiple
collections
 Pathogens: Strep viridans, S. aureus,
Strep pneumoniae, enterococcus.
 IV drug abusers: S. aureus

Hypertension
In primary hypertension, lab results can
be normal.
 Abnormalities may include:
 UA: hematuria, proteinuria, casts
 Lytes: potassium abnormalities
 FBS: screen for diabetes, metabolic
syndrome.
 Lipids: screen for atherosclerosis risk

Other Lab tests
PT - Prothrombin Time
 Includes INR - International Normalized
Ratio
 Used to monitor Coumadin therapy
 PTT - Partial Thromboplastin Time
 Used to monitor Heparin therapy (not
used with LMWH)

Case Study #2

47yo female admitted with cc of
increasing SOB and fatigue. Past
medical hx: cardiac arrhythmias, heavy
alcohol consumption for many years
and 40 pack year smoking history.
Case Study #2
PE: A&O, BP 100/65, HR 96, T 97.5F,
RR 23.
 Exam of neck showed distended jugular
veins. Abdomen: protuberant abdomen
with ascites. Liver and spleen not
palpable. Pitting edema of LE.

Case Study #2
ECG: Sinus tachycardia and nonspecific S-T segment changes.
 CXR: No pulmonary infiltrates, no
masses. Enlarged heart.
 Labs?
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