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Diagnostic Medicine > Introduction to cardiovascular Diagnostic Testing > Flashcards

Introduction to cardiovascular Diagnostic Testing Flashcards

1
Q

Why do we order diagnostics?

A
  • To establish the presence or absence of illness, disease, condition, injury or other pathological state.
  • Rule in primary diagnosis
  • Rule out differential diagnoses
  • Risk stratification
  • Assess for comorbidities
  • Assess for response to therapeutic intervention
  • Assess for adverse reaction to therapeutic intervention
  • Screening purposes
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2
Q

Categories / types of cardiovascular diagnostic studies

A
  • Laboratory
  • Radiology
  • Electrocardiography / Electrophysiology
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3
Q

What do you have to consider when determining what type of lab testing should be done?

A
  • Outpatient / emergency / inpatient
  • Time frames for receiving testing results
  • i-Stat(2-10 minutes)
  • Seconds to 10+ days

Outpatient lab stat request consideration

CBC w/ diff, CMP, Lipid Panel w/ reflex LDL direct, cTnI, CK w/ reflex to isoenzymes

Critical values

Sample availability

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4
Q

Describe the pre-test and post-test probability in relation to the Prevalence of CVD (Cardiovascular Disease) and the factor of age

A

Ex: There is a low probability that someone in the age range of 20-39 would have hyperlipidemia so they would have a low pre-test probability. If this person is older, they would have a high post test probability.

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5
Q

What is the most prevalent tupe of Cardiovascular Disease?

A

Coronary Heart Disease (48%)

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6
Q

Coronary Heart Disease

A
  • Primary cause of death and disability in the US
  • 1 out of 5 deaths in US
  • Every 25 seconds someone will have a myocardial infarction
  • Every minute someone will die from a myocardial infarction
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7
Q

Non-modifiable risk factors for CVD

A
  • Age
  • Gender
  • Family History
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8
Q

Modifiable risk factors for CVD

A
  • High Blood cholesterol
  • High Blood Pressure
  • Physical inactivity
  • Obesity and Overweight
  • Smoking
  • Diabetes
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9
Q

Cholesterol

A

Essential substance required for synthesis of:

  • Cell membranes
  • Steroid hormones
  • Multiple other compounds utilized in daily physiological processes
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10
Q

Triglycerides

A
  • Glycerol + three fatty acids = 1 triglyceride
  • Energy source (primarily aerobic exercise)
  • Energy storage
  • Transported through blood within lipoproteins
  • Chylomicrons and VLDL have greatest concentration
  • Stored in skeletal muscle and adipose tissue
  • Elevated in a non-fasting state → nothing to eat or drink other than water for 8 to 10 hours
  • No coffee
  • No chewing gum
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11
Q

Lipoproteins (VLDL, IDL, LDL, HDL)

A
  • Lipid and protein structures
  • Transport cholesterol and triglycerides
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12
Q

Chylomicrons

A

-Transport dietary exogenous triglycerides (TG) and cholesterol from the intestines to the liver

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13
Q

VLDL

A
  • very low density lipoprotein
  • Transport TG & cholesterol from liver into circulation
  • Pre-cursor of IDL and LDL
  • Contain
  • Triglycerides
  • Cholesterol
  • Apolipoprotein B (Apo B 100)
  • Atherogenic particle (B for BAD)
  • Linked to pathologic affects of hyperlipidemia
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14
Q

IDL

A
  • intermediate density lipoprotein
  • Transport TG & cholesterol within circulation
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15
Q

LDL

A
  • low density lipoprotein
  • Transport TG & cholesterol within circulation
  • Enriched with cholesterol
  • Small enough to enter cells
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16
Q

HDL

A
  • high density lipoprotein
  • Transport endogenous cholesterol from the tissues to the liver
  • Densest and smallest of lipoproteins
  • Contains Apolipoprotein A-1 (ApoA-1)
  • A is better than B
  • Responsible for reverse cholesterol transport
  • Anti-atherogenic
  • Termed “good / healthy cholesterol”
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17
Q

Total Cholesterol

A

HDL + VLDL + LDL

18
Q

Atherogenesis

A
  • Fatty material and plaque are deposited in the wall of an artery
  • Narrowing of lumen
  • Eventual impairment of blood flow
  • Excess cholesterol (VLDL and LDL) starts process
  • Abnormal cholesterol metabolism
  • Genetic
  • Insulin resistance
  • Dietary intake
  • Saturated fats/ trans-fats
  • Dietary cholesterol
  • Obesity
19
Q

Hyperlipidemia - Laboratory Evaluation

A
  • In fasting serum, cholesterol is carried within:
  • VLDL, LDL, and HDL molecules
  • Total cholesterol equals the sum of these three components:
  • Total Cholesterol = HDL + VLDL + LDL
  • Most clinical laboratories measure total cholesterol, triglycerides, and HDL
  • LDL and VLDL are more difficult to measure and are thus commonly calculated as an estimate
20
Q

Friedewald equation

A

Total Cholesterol = HDL + VLDL + LDL

[LDL-chol] = [Total chol] - [HDL-chol] - ([TG]/5)

  • The Friedewald equation should not be used under the following circumstances:
  • When chylomicrons are present which means that the patient should be fasting for 8 to 10 hours
  • When plasma triglyceride concentration exceeds 400 mg/dL
  • Specialized lab test must be utilized to determine LDL
  • Fasting lipid panel vs.
  • Fasting lipid panel w/ reflex to LDL direct
21
Q

Hyperlipidemia: Normal ranges for adults

A
  • Total cholesterol < 200 mg/dl
  • LDL cholesterol < 130 mg/dl
  • HDL cholesterol > 40 mg/dl
  • VLDL cholesterol < 30 mg/dl
  • Triglycerides < 150 mg/dl
22
Q

Creatine Kinase (CK or CPK)

A
  • Enzyme contained in the heart muscle, skeletal muscle and brain
  • CK – MM (skeletal muscle)
  • CK – MB (heart muscle)
  • Rise 4-6 hours , peak 18-24 hours, normalizes 48-72 hours
  • CK – BB (brain)

CK – MM 94-100%

CK – MB 0-6%

CK – BB 0%

Creatine kinase (CK) aka (CPK) is an isoenzyme found in skeletal and cardiac muscle, brain and lung. The isoenzymes are defined as follows:

  • CK-MM is skeletal muscle
  • CK-MB is cardiac muscle
  • CK-BB is brain and lung tissue

In a “normal” healthy individual there is always remodeling of skeletal muscle so that is why the normal value is 94-100%, at times there can be some breakdown of cardiac muscle which is why the CK-MB can range from 0-6%, rarely if ever is there enough breakdown of brain or lung tissue to cause elevation of the CK-BB so it almost always 0%

In the setting of an MI the increased breakdown of cardiac tissue results in elevation of the CK-MB levels which causes it to become more detectable in the blood so the percentage level increases. If all of the numbers need to add up to 100% it should make sense that the skeletal muscle percentage drops down to 85% due to the CK-MB rising to 15%.

  • CK – MB
  • Rise 4-6 hours , peak 18-24 hours, normalizes 48-72 hours
  • Sensitivity of 56% and specificity of 45%
23
Q

Myoglobin (MB)

A
  • Iron and oxygen binding protein found in muscle tissue
  • When cardiac muscle cells are damage myoglobin is released into the blood stream
  • Rise in 2-4, peak 6-12, normalize 24-36
  • Sensitivity of 83% and specificity of 99%
24
Q

cTroponin I & T

A
  • Regulatory proteins found in skeletal and cardiac muscle
  • Troponin I more specific for acute myocardial infarction (AMI) than Troponin T
  • hs-cTnI sensitivity 99% / specificity 89%
  • Increases within 2-6, peak 18-24 hours, hours and normalizes in 7-14 days
  • ~80% w/ 2-3 hours ED arrival
  • Recommend serial monitoring*
  • Improved sensitivity and specificity compared to older biomarkers

cTroponin I & T

  • <0.04 Normal
  • 0.04 – 0.39 Elevated above the 99th percentile of a healthy population
  • > 0.4 probable MI
25
Q

B-type Natriuretic Peptide (BNP)

A
  • Secreted primarily by the ventricular myocardium in response to wall stress
  • Ventricular volume expansion
  • Pressure overload
  • Validated as a marker for CHF
  • <100 pg/mL – CHF can be excluded
  • 100 – 400 pg/mL – inconclusive
  • >400 pg/mL – consistent with CHF
  • Sensitivity 90% / specificity 73%
  • Some studies have demonstrated that BNP may also be a useful prognostic indicator post MI
  • Significant elevation of BNP post MI associated with decreased left ventricular ejection fraction
26
Q

High Sensitivity C-Reactive Protein

(hs-CRP)

A
  • Abnormal protein that appears in the blood in the acute stages of various inflammatory disorders
  • Elevated hs-CRP is associated with an increased risk of CVD
27
Q

PT/INR

A
  • PT is a coagulation test that measures the time it takes to form a firm fibrin clot after thromboplastin (factor III) and calcium are added to the serum sample.
  • The findings are expressed in terms of seconds or as a percentage of normal activity.
  • Prothrombin time (PT) is also expressed in terms of the INR using standardized thromboplastin reagents.
28
Q

D-Dimer

A
  • Injury to a vein or artery activates the coagulation cascade, creating a blood clot.
  • Fibrin threads are produced and cross-linked, forming a net to catch platelets
  • Plasmin breaks down the clot for removal.
  • Broken fibrin fragments are termed fibrin degradation products (FDP)
  • One of the which is D-dimer
  • High sensitivity but low specificity
29
Q

Electrocardiography (ECG)

A
  • Disorders of rate and rhythm
  • Myocardial ischemia / injury
  • Electrolyte imbalances
  • Structural changes
  • Conduction disturbances
30
Q

Ambulatory Monitoring

A
  • Assess for silent ischemia
  • Asymptomatic patient with history of ischemia or MI
  • Assess efficacy of antidysrhythmic medications or following the discontinuation of antidysrhythmic
  • Palpitations*
  • Unexplained weakness, fatigue, dyspnea, dizziness or syncope
  • Pacemaker function
31
Q

Exercise Stress Test

A
  • Measures heart’s response to exercise while a patient exercises following a specific protocol
  • ECG
  • Myocardial perfusion imaging (“nuclear stress test”)
  • Echo
32
Q

Chemical Stress Test

A
  • Indications
  • Unable to exercise
  • Poor motivation
  • Stimulates physiological state
  • Medication supplied until 85% of age predicted max
  • Dobutamine
  • Adenosine
33
Q

Intracardiac Electrophysiology Study (EPS)

A
  • Internal ECG
  • Detection and recording of timing and conduction of electrical impulses
  • Induce arrhythmias and see where they originate
34
Q

Myocardial Perfusion Imaging

A

•Scintigraphic studies (administration of a radionuclide tracer and imaging with a gamma camera)

35
Q

Echocardiography

A
  • Ideal for assessing structure and function
  • Chamber size
  • Wall thickness
  • Function
  • Ejection fraction
  • Direction and velocity of blood flow
  • Wall motion
  • Stress test
  • Valvular abnormalities
  • Congenital abnormalities
  • Pericardial effusion
36
Q

Transesophageal Echocardiography

A
  • Utilized to evaluate posterior structures
  • Atria
  • AV valves
  • Portions of aorta
37
Q

Computed Tomography (CT)

A
  • Not the best for cardiac structures
  • Myocardium, chambers, valves
  • Very good for vessel imaging (aorta)
  • Newer uses
  • Calcium score (CCT) – no contrast
  • Angiography (CCTA) – contrast
38
Q

Cardiac MRI

A
  • Previous limitations are being overcome and now becoming utilized on a more frequent basis
  • Follow up to echo (valvular, congenital, wall)
  • Morphology, function, perfusion, viability, vascular anatomy (MRA)
  • Primary limitation is availability and need for authorization
39
Q

Cardiac Catheterization & Angiography

A
  • Cardiac catheterization and angiography, although invasive procedures, remain invaluable in the management of most patients with congenital and valvular heart disease, as well as coronary artery disease.
  • Right heart catheterization allows measurement of right atrial, right ventricular, pulmonary artery and pulmonary capillary wedge pressures, oxygen saturation, and cardiac output.
  • Left heart catheterization is performed to assess the cardiac valves and left ventricular function.
40
Q
A

Diagnostic Medicine (8 decks)

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