cardio labs Flashcards
vascular disease
all organs and tissue are potential targets of injury in vascular disease
blood vessel diseases
-Atherosclerosis
-HTN
-Vasculitis (inflammation)- autoimmune, infection -> can cause stroke (w/o any common risk factors!)
-Aneurysms
-Tumors- increase vascular supply to grow
-DVT
-PE
-Stroke
Causes of atherosclerotic ds
Ingestion of excess fats in diet: MC
Primary Lipid disorders
- intake, genetics
Secondary Lipid disorders
- pancreatitis
- hypothyroidism, nephrotic syndrome, liver disease, diabetes, obesity, and alcohol abuse
atherosclerosis: fasting lipid profile; what values are high
Need 8-12hr fast for blood draw
-Total Cholesterol - >200 (high)
-LDL- >200 (high) -> friedwald formula or direct assay
-HDL- you want it > 40
-Triglycerides- >190 (high)
-numbers diff by age, risk factors, gender
LDL values
> 200 mg/dL is elevated
- Know LDL values in term with a clinical picture
~ 70 mg/dL in cardiac patients (recommended) QT
Friedewald Formula or direct assay*
pharm note:
- ideal is under 100
- high is greater than 160
lifestyle modifications: how to lower elevated LDL
-exercise
-smoking cessation
-target BMI
-diet
screening and managing hyperlipidemia chart: when to get fasting lipid profile?
-Triglycerides (TG) >250 mg/dL (>6.5 mmol/L).
-HDL cholesterol (HDL-C) <40 mg/dL (<1 mmol/L).
-Hx of hypertriglyceridemia
- On medications that elevate triglycerides (like estrogens, glucocorticoids).
- DM
- Fam Hx of genetic hyperlipidemia
next step: estimate cardiovascular risk with calculator and see if tx is warrented
- below threshold for tx: reassess lipids in 5 yrs
- near threshold: reassess in 3 yrs
- above threshold: tx high LDL and repeat LDL-C 6 wks post-tx and then every 6-12 months
total cholesterol
TC = HDL + LDL + VLDL + IDL + Lp
- over 200 = elevated
-non specific
-is good cholesterol elevated?
-is bad cholesterol elevated?
-you never just look at this value
HDL
Target > 40 mg/dL
Low levels represent a cardiac risk factor
> 60 reduces cardiac risk!
Triglycerides, when is it elevated?
> 190 mg/dL: elevated
Elevated in:
- pancreatitis*
- hypothyroidism
- nephrotic syndrome
- liver disease
- metabolic disorders
- toxemia
“can study for it before lipid panel” - more variable dependent on what you eat
framingham score: what factors
-gold standard cardiovascular risk
-HDL is the only protective factor -> reduces risk of atherosclerotic disease
-memorize factors
- if they are on meds with HIGH BP -> uncontrolled*
Factors: “THAH Gold Standard”
- Total Cholesterol
- HDL
- Age
- HTN
- Gender
- Smoking
clinical picture flow chart
-clinical ASCVD- CAD, MI, PAD, cerebral vascular disease, carotid disease, renal artery stenosis
-primary prevention- preventing the first event
-secondary prevention- preventing a second even from happening
-know this chart
Secondary prevention: ASCVD
Very high risk (multiple major ASCVD events or one major ASCVD event plus multiple high-risk conditions),
- goal: MAX tolerated statin to achieve a 50% or more reduction in LDL-C
- if LDL-C levels are ≥70 mg/dL on statin: add ezetimibe -> add CSK9 inhibitor
stable ASCVD and less intensive risk factors:
- High intensity statin: > 50%
- moderate intensity: 30-49%
primary prevention: intermediate LDL + no diabetes
40-75 yrs + LDL-C levels of 70-189 mg/dL without DM:
- risk of ASCVD within 10 years is done to determine the intensity of statin therapy
High Risk (≥20%):
- High-intensity statin aiming for ≥50% LDL-C reduction.
Intermediate Risk (7.5-19.9%):
- Moderate-intensity statin with a goal of 30-49% LDL-C reduction
Borderline Risk (5-7.4%):
- Risk discussion for statin benefits
- consider moderate-intensity statin if risk enhancers are present
Low Risk (<5%):
- Lifestyle changes
- statins based on individual risk factors.
primary prevention: LDL > 190 mg/dL
tx: maximally tolerated statin
- if LDL > 100: add ezemtimibe -> PCSK9
What is the recommended statin therapy for individuals aged 40-75 with diabetes?
Start with a moderate-intensity statin
- possibility of escalating to high-intensity statin (50+ yrs, ASCVD risk factors)
Target: LDL-C reduction of 30-49% or ≥50% for those at higher risk.
statin ADR
-muscle cramps
-elevated LFTs- 6 weeks lipid levels, and LFTs
-statins attack endogenous LDL- genetic cholesterol
-ezetimibe stops LDL absorption
C-reactive protein
Persistent inflammatory process!
Increased risk of cardiovascular events based on CRP:
- <1.0 mg/L low risk
- 1-3 mg/L intermediate
- >3.0 mg/L high risk
- pts with inflammatory process will have CRP > 3
-Used to classify those patients who are at borderline CV risk
-is this due to vasculitis?
metabolic syndrome
-Series of risk factors for cardiovascular disease ( MI, CVA, DM), kidney dysfunction,
- occurs 40% of US pts over 60 years of age!
-May not have any physical symptoms!!!
metabolic syndrome criteria
At least 3 of the following:
-impaired glucose tolerance (pre-diabetes): fasting plasma glucose >=100 or A1c 5.6-6.4
-abdominal obesity
-hypertriglyceridemia- >=150 or on on meds for it
-low levels of HDL: <40 (men), <50 (women), or on meds for it
-HTN- >130/85, or on meds for it
DUTCH dx criteria for familial/genetic hypercholesterolemia
6– Family hx of early heart disease or high cholesterol
- Clinical hx of premature CAD
-PE: tendinous xanthomata (yellow plaque) or corneal arcus (greyish ring around the eye) before a certain age
- Elevated LDL-C.
- DNA analysis revealing a functional mutation in relevant genes such as LDLR, apoB, or PCSK9.
higher score = more likely FH
->8: DEFINITIVE dx
-6-8: probably dx
- 3-5: possible dx
Cardiovascular risk factors
-Smoking,
-Hypertension
-DM
-Obesity
-Physical inactivity
-Family History of coronary disease
HTN: how common is it? correctable causes of HTN
In US: up to 50% of adults have HTN
Correctable causes of HTN:
-obesity
-tobacco
-Na+ intake*
-ETOH
-oral contraceptives
-NSAIDS
HTN complications + secondary HTN
Microvascular damage
-chronic HTN can affect GFR / kidney function
Secondary: HTN caused by an underlying ds
-renal artery stenosis
-pheochromocytoma
-hyperaldosteronism
-hypothyroidism
vasculitis
Definition: inflammation of the blood vessel wall
-decrease blood flow -> necrosis of tissue
- associated with autoimmune rxns: antineutrophil cytoplasmic antibody, elevated ANA
- MC presentation = skin changes and modeled lacy skin pattern
- different forms of vasculitis are classified by the size of the vessels affected
Primary: no underlying ethiology
Secondary:
- due to infection (HIV, Hep B, Hep C,
- due to autoimmune (lupus, RA):
dx of vasculitis
Dx:
- Presence of characteristics of particular clinical findings
-Inflammation within particular size blood vessels
- vessel bx + labs help dx
Labs:
-ANCA antibodies IgG (dont need to know this): systemic vasculitis
-Elevated erythrocyte sedimentation rate (ESR)
-C-reactive protein
-End organ damage
-antineutrophil cytoplasmic antibody, ANA
vasculitis sx
-mottled, lacey, palpable purpura
-livedo reticularis
-fever, headache, wt loss
-joint pain
-GI- bloody stool, ab pain
-heart- MI, HTN
-stroke- if pt comes in with suspected stroke -> and the c-reactive protein, ANA, ESR -> suspect vasculitis
-eye- reduced visual acuity
-nose bleeds
-lungs- bloody cough, infiltrates
-kidneys- glomerular nephritis
DVT/PE
DVT: blood clots in veins in legs and can lead to PE in arteries
D-Dimer:
-Cross linked fibrin generation
-Elevated in setting of DVT/PE however not specific!
-Can help to rule out only: negative results = NO PE
-is there a hypercoagulable state?
stroke
Work-up:
-No diagnostic lab for stoke, no organ marker
-Hypercoagulable work up: check PT/INR, PTT**
-initiate anti-platelet therapy
Ischemic stroke: blood supply cut off
- MC
- caused by atherosclerosis, Antiphospholipid syndrome (prothrombotic condition), thrombus, TIA, emboli
Hemorrhagic: lack of blood flow due to hemorrhage
- HTN: weakens arteries over time
- AV malformations
- Brain aneurysms
acute coronary syndrome event flow chart (low risk)
Ischemic chest pain pattern- STEMI, NSTEMI, unstable angina
1) manage them assuming ACS: do a EKG within 10 minutes, get troponin levels, BMP, chest xray
2) check troponin levels - yes = tx; no = move to next step
3) calculate the HEART pathway risk score:
- Score: 0 = noncardiac chest pain
- score 1+: need to obtain 2ND TROPONIN 3H after 1st one -> yes = tx; no = move to next step
4) recalculate HEART risk score
- 0-3: evaluate other causes of chest pain
- 3+: need to obtain a non-invasive eval prior to discharge
overview of approach for suspected acute MI in ED
pt comes in with pattern of MI chest pain
1) manage them assuming ACS: do a EKG within 10 minutes, get troponin levels, BMP, chest xray
TIMI score
The TIMI Risk Score for UA/NSTEMI estimates mortality for patients with unstable angina and non-ST elevation myocardial infarction (MI).
HEART score for chest pain
SCORE:
- tells you the risk of major adverse cardiovascular events for chest pain pts in the ED
Values:
-0-3- low risk
-4-6- intermediate
->7- high risk
cardiac biomarkers for MI
Cardiac troponin*
-serial rise in troponin
-elevation for days after MI
- acute rise and fall pattern*
-all other biomarkers of nonspecific and not helpful
DDx: high troponin due to non-MI/ACS
- will have ambiguous pattern of troponin change
troponin
-Only marker used to diagnosis a Myocardial Infarction!
-Normal value is <0.01 ng/ml: + troponin = above the threshold
-rises within 2-4 hrs*, peaks 10-24 hrs, drops within 1-2 weeks
-Can calculate size or evolving MI (higher troponin = higher area of infarction)
-Used in conjunction with clinical signs
-dont need to know numbers
-cardiac troponin I and cardiac troponin T
-high sensitivity troponin assays have cut off that is 99th precentile of cardiac disease-free reference population
other causes for troponin elevation
-cardiac surgery
-cocain- vasospasms
-PE, stroke
-hemorrhage
DDx: high troponin due to non-MI/ACS
- will have ambiguous pattern of troponin change
other markers
Poor Specificity because of wide tissue distribution:
-Aspartate Aminotransaminase (AST)
-Creatine phosphokinase (CK)
-CK-MB*
-Myoglobin
-Total lactate dehydrogenase (LDH)
CK and CK-MB
Creatine kinase (CK) and its myocardial isoenzyme (CK-MB) -> used to be MC serologic tests for dx of MI prior to troponin
- idea: muscle damage: CK enzymes will be released into bloodstream but it may also present in skeletal muscle (non-specific)
-not really used anymore
-Many institutions no longer offer CK-MB testing
-some use CK-MB for detection of early reinfarction, although not guideline recommended
CK and CK-MB: why is it not used anymore?
why is it not used:
-Elevations in total serum CK lack specificity for myocardial damage, which improves with measurement of the MB fraction
-normal range of CK VARIES; a twofold or greater increase in the CK concentration is required for dx; issue with pts with low muscle mass
Criterion can be problematic in older individuals with lower muscle mass:
- may have low baseline serum total CK and, during MI, may have elevated serum CK-MB with values of total CK that rise but REMAIN WITHIN NORMAL RANGE
rhabdo + CK levels
Rhabdomyolysis: hallmark = elevation in CK and other serum muscle enzymes (5x upper limit of normal)
-causes: sustained exercise, compartment syndrome, crush injury
CK levels:
-Serum CK levels at presentation: range from approximately 1500 to over 100,000 international units/L
-rise: within 2 to 12 hours following the onset of MUSCLE INJURY and reaches its maximum within 24 to 72 hours
- Decline: 3-5 days after cessation of muscle injury
Serum half-life: 1.5 days and declines at a relatively constant rate of about 40 to 50 percent of the previous day’s value
- In patients whose CK does not decline as expected -> concern for continued muscle injury or the development of a compartment syndrome
myoglobin
Myoglobin =ubiquitous heme protein that is rapidly released from damaged tissue because of its small size
- half-life in plasma: 9 minutes (early)
-Due to its early appearance in the serum, myoglobin was postulated to be a useful adjunct to either troponin or creatine kinase MB (CK-MB) for the early diagnosis of myocardial infarction (MI)
-With highly sensitive cardiac troponin (cTn) assays and the use of the 99th percentile or 10 percent coefficient of variation cut-off, cTn is elevated PRIOR to elevations in myoglobin
summary:
- used to use myoglobin for MI because it was an early biomarker
- now: troponin shows up even faster and its not used anymore
- MYOGLOBIN USE IS IN RHABDOMYOLYSIS
lactate dehydrogenase
Commonly used in the past in combination with AST and CK-MB to diagnose an acute MI
- LDH: enzyme found in all parts of the body
-LDH consists of M (muscle) and H (heart) subunits that give rise to five isoenzyme
- heart: LD1 and some LD2
- Red cells, kidney, stomach, and pancreas are other important sources of LD1
- LD5: skeletal muscle and liver.
LD levels with MI:
- rises to abnormal levels 10 hours after the onset of MI
- peaks at 24 to 48 hours
- remains elevated for six to eight days
Troponin = more specific than LD and remain elevated for 5 to 10 days
- current recommendations suggest that LD no longer has a role in the diagnosis of MI
congestive heart failure description, how common is it, mortality, hospitalizations etc
-only cardiovascular disease with INCREASING incidence
-leading cause of hospitalizations in pts 65yo and older
-5 mil pts with CHF, 400,000 new cases each year
-5 year mortality 10% mild CHF- 80% end stage disease
Definition: ineffective pumping of heart leading to accumulation of fluid in the lungs
monitoring CHF
Brain natriuretic peptide, BNP and BT-proBNP
-released due to myocardial stress or fluid overload
-Filling pressure defect
-BNP = chronically elevated with acute elevation in setting of volume overload in CHF patients
-Ordering a BNP in patients with shortness of breath can reduce uncertainty of diagnosis
-normal BNP: dx of CHF is highly unlikely
-useful for long term monitoring in guiding therapy, monitoring course of disease and risk stratification
BNP
Normal Range:
- 5–1,300 pg/mL.
Levels above 400 pg/mL:
- indicates HF in patients with SOB
Levels below 100 pg/mL:
- high negative predictive value for HF
- HF is unlikely if BNP is below this level
-Difference by age, sex, BMI
-Elevated in renal failure
-Equivalent to or better predictor than CXR and P/E
-Correlates with NYHA Class
-Patients in the highest 25% have greater mortality at 2 years then those in lowest 25%
-Can not be used with Entresto
pro-BNP
Age ranges for HF diagnosis
-<50yrs: HF at 450 pg/mL
-50-75 yrs: HF at 900 pg/mL
->75 yrs: HF at 1800 pg/mL
-It has a longer half-life than BNP and is considered to have greater prognostic value regarding left ventricular function
-Difference by age, sex, BMI
-Elevated renal failure
common triggers of elevated BNP and NT-proBNP
DECKS IN CLIN LAB CLASS (8)
