Week 12 Flashcards
difference between primary and secondary hypertension
primary - essential hypertension - no identificable cause - genetic and lifestyle related
secondary - underlying condition renal artery stenois, endocrine disorders, (hyperaldosteronism or Cushings) or medications like corticosteriods or NSAIDs)
silent killer
Severe Hypertension (Hypertensive Crisis)- headaches, visual disturbances, chest pain, shortness of breath, and organ damage (e.g., acute kidney injury, retinopathy, heart failure).
how is hypertension caused
increased cardiac output- hypervolemia -excess fluid in the blood or increased heart rate = high BP
Increased peripheral resistance - vasoconstriction or changes in arterial wall which will need higher pressure to maintain flow
what are tests you can do for hypertension
BP measurement above 140/90
make sure you have proper technique, cuff size, and pt positioning
Electrolytes and Renal Function Test- lyt5 and urea
urinalysis - proteinuria or hematuria = kidney damage
What is systolic heart failure
HF with reduced ejection fraction HFrEF- when left ventricle cant contract so there is reduced ejection of blood
What is diastolic heart failure
HF with preserved ejection fraction HFpEF
when left ventricle is stiff and cant relax so it cant fill with blood
What does the body do in response to reduced cardiac output
Neurohormonal activation
-activation of sympathetic nervous system and RAAS= vasocontriction, fluid retention and increased afterload = WORSE HF
Cardiac remodeling = hypertrophy and fibrosis
how does HF manifest
-Dyspnea (shortness of breath),
- exertion or when lying down
(orthopnea)
fatigue
peripheral edema (swelling of the legs and ankles)
-rapid weight gain due to fluid retention.
- Signs: Elevated jugular venous pressure, pulmonary crackles, and an S3 gallop (a third heart sound indicating increased ventricular filling pressure).
how do you monitor HF
Echocardiography - cardiac structure and function
BNPs
regularly monitor pts on diuretics and RAAS inhibitors to prevent hypokalemia and renal dysfunction
Arrhythmias and how can they happen
symptoms
-irregular heart rhythm
re entry circuits- abnormal electrical pathway
triggered activity - abnormal action potentials because heart muscle was repolarized
automaticity - abnormal pacemaker outside the SA node
palpitations, dizzy, syncope
can be asymp
can lead to stroke , A FIB because of thromboembolism
how do you diagnose and monitor arrhythmias
-ECG -primary tool for diagnosis , holter monitoring (make sure the equipment is calibrated and interpreted well)
-electrophysiological tests - invasive tests to map heart electrical activity to find the source of the arrhythmia and guide ablation therapy
-monitor K and MG
Dilated Cardiomyopathy (DCM)
- chambers become enlarged (dilated) and weakened, leading to systolic dysfunction
-Impaired Contractility
-Myocardial Fibrosis- stiffening
-can be caused by mutations, viral infections, toxins like alcohol and autoimmune diseases
Hypertrophic Cardiomyopathy (HCM)
-abnormal thickening (hypertrophy) of the heart muscle = in the interventricular septum.
–Myocardial Fibrosis- stiffening
-inherited
-can cause diastolic dysfunction = higher risk of arrhythmias
Restrictive Cardiomyopathy (RCM):
-heart muscle becomes rigid
-restricted filling during diastole
-Myocardial Fibrosis- stiffening
amyloidosis, sarcoidosis, and fibrosis due to radiation or chemotherapy
What are the Complications: of D/H/Rcm
Heart failure, arrhythmias, thromboembolism, and sudden cardiac death
how do you diagnose and monitor
Cardiomyopathies
Echocardiography- best for cardiomyopathies lets you know chamber size, wall thickness, systolic and diastolic function
Cardiac MRI- looks at fibrosis and scarring
look at BNPs, TNIHS for assessing severity and response to treatment
Genetic testing for familial cardiomyopathies
what do you need for an accurate diagnosis of cardiovascular condition
echocardiography - uses ultrasound waves to create images of the heart
cardia MRI and CT - images of heart and blood vessels good for looking at structural abnormalities
-Gadolinium-enhanced MRI for detecting myocardial fibrosis and viability
holter monitoring - portable device for 24-48 hours
Medications to manage and treat cardiovascular diseases
Antihypertensives: ACE inhibitors, beta-blockers, calcium channel blockers.
o Antiplatelets and Anticoagulants: Aspirin, clopidogrel, warfarin for preventing thromboembolic events
o Statins: For lowering cholesterol levels and reducing the risk of CAD.
clinical indications for therapy
manage hypertension when pts have blood pressure >140/90
statins for primary and secondary prevention when pts have increased LDL
make sure BP and lipidsi LIP2R are regularly measured and therapy is adjusted
INR monitoring if pts are on warfarin to make sure they arent on bleeding risk
Ddimer - for DVT and PE
Cardiac enyzmes - TNIHS, CKMD - myocardial injury
hemolysis and lipemia can impact the tests
What is troponin used for
Diagnosis in Acute Myocardial Infarction (AMI) - increased with ECG findings
Assess risk for Acute coronary syndrome
Monitoring Cardiac Injury or PCI
Increased in myocardial stress , sepsis, pulmonary embolism and renal failure
how are High-Sensitivity Cardiac Troponin (hs-cTn) Assays completed
-detect very low levels
-earlier diagnosis of AMI
standard assays are less sensitive
use sandwich ELISA-antibodies
specific to different epitopes of the troponin molecule capture and detect the analyte
-detection with labels like enzyme linked or chemiluminescent detection - signal is proportional to concentration
are POCT used for troponin
yes in critical departments like ER
- immunochromatographic methods
-need careful validation and regular QC
-quick TAT - early diagnosis for AMI
-good for remote areas
-reduced preanalytical errors because there is no need to transport, centrifuge or mix, less misdiagnosis
-better work flow
-shorten wait time
-quicker rule out or rule in of myocardial infarction especially when used with accelerated diagnostic protocols (ADPs)
-rules out pt that arent having heart trouble so they can be discharged
Pre/Post-Analytical Variables for TNIHS
hemolysis, improper mixing or inadequate anticoag
trop levels rise in 3-4 hours after myocardial injury , peak at 12-24 hours and stay high for two weeks
-timing of collection is needed for accurate interpretation
Post
interpretation
false pos/neg can occur due to analytical interference, biological variation or improper interpretation of RI
What are the disadvantages for POCT for thins
-low sensitivity and specificity can cause false pos = too many admissions or false neg= missed AMI diagnosis
Constant QC- too many people with different types of training use it, operator variability
higher cost per test - this can limit use
limited test throughout - one at a time instead of multiple tests at time like in a lab .This may not be good in a busy environment like the ER
Operator related errors- improper use, sample application or timing can affect testing accuracy and reliability
Variability - POCT are more prone to interference - hemolysis, lipemia, bilirubin = false interpretations
What is CKMB used for
Creatine Kinase-Muscle Brain subunit or CK-2 isoenzyme)
-no longer the primary biomarker for MI but still good when trop isnt available
AMI diagnosis - rises 3-6 hours after mycardial injury, peak at 12-24 hours and back to baseline in 48-72 hours so its good for detecting reinfarction or new injury after the initial one
-assessment of reinfarction because the levels baseline faster than trop, another rise another MI
-when trop is increased because of other conditions like renal failure or heart failure CKMB is an additional marker for AMI
-can be used when POCT or trop isnt available
how is CKMB measured
immunoassay for CKMB isoenzyme - use ABs to target CKMB
-use of sandwich ELISA, use monoclonal AB to bind CKMB and detect concentration with colorimetric, fluorescent, or chemiluminescent signals.
Electrophoresis - can seperate CK isoenzymes based on charge and migration pattern
POCT- immunochromatographic method
Pre/ANA/post analytical issues with CK measurement
Pre
-hemolysis- false increase there is CK in RBC
-Timing- important to look at peak levels
Ana-
isoenzyme interference
-non cardiac isoenzymes like those present in skeletal injury can interfere with CKMB assay
Post
result interpretation
Advantages for CKMB detection
Early detection of myocardial injury
-levels rise quickly (3-6 hours) after heart injury which can help with early diagnosis where TNIHS is not available
Detects Reinfarction
-since levels baseline in 48-72 hours it can help detect if there was a repeat injury which can be hard with TNIHS
What are the disadvantages to CKMB
Lower detection than TNIHS
-ckmb less specific for cardiac events then TNIHS, it can be increased in skeletal muscle injury, after excersise or muscle diseases = false positive
Limited sensitivity
-cant detect EARLY heart injuries or EARLY infractions like TNIHS = delay in diagnosis
Less favorable kinetics for monitoring of prolonged injury
-because baseline returns quickly it cant do long term monitoring like TNIHS which is elevated for days
why is TNIHS better than ckmb
-higher specificity for Myocardial injury
TNIHS is specific to the heart and isnt found in other tissues like ckmb which means that once TNIHS is increased its due to the heart = less false positives
-greater sensitivity and accuracy
TNIHS assays are very sensitive = greater accuracy and earlier diagnosis - faster interventions
Longer diagnostic window for detection
- TNIHS levels stay up for longer after heart injury (1-2 weeks) which means that you can detect a heart injury even if the patient is late in experiencing the symptoms
What is BNP and NT-BNPS
-biomarkers in diagnosis and management of HF
-released in response to volume expansion and increased wall stress = good for differentiating if its a cardiac or lung condition
When is BNP released
-produced in ventricles of the heart
-released when heart muscle cells -myocytes stretch because of pressure or volume overload like HF
-promotes vasodialtion, natriuresis (excretion of NA in urine) and diuresis (increased urine production) = lowering blood volume and workload
When is NT proBNPS released
-inactive fragment
-proBNP split into BNP and NT proBNP (no biological activity but half life is used for assessing HF)
how to differentiate HF from lung disease
-dyspnea occurs in both HF and lung conditions like chronic obstructive pulmonary disease (COPD), pneumonia, and pulmonary embolism
- Increased BNP or NT BNPs indicate HF more than lung
how do BNPs and NTBNP help with risk stratification
-if both elevated then it correlates with severity of HF
-the higher the values the worse the outcomes
how can BNPs and NTBNP help to guide treatment
-can help tell the effectiveness of treatment
-a big reduction means that the treatment is working = pt is getting better
Helps to predict prognosis- if your levels are consistently high despite treatment then youre not getting better and treatment needs to change
BNP >400 heart failure <100 - no HF
NTBNP >300 HF possible and <300 no HF
>1800 HF likely
how is BNP tested
immunoassay like chemiluminescent immunoassays or fluorescence immunoassays
-antibodies that specifically bind to BNP
how is NT BNP tested
immunoassays
used more often because of its higher half life and stability in blood - reduction of variability and increased reliability
why is it important to distinguish between heart and lung problems
if pt have just dyspnea its hard to differentiate which issue is causing it
-helps with targeted treatment HF conditions work on reducing fluid overload whereas for the lung we give alot of steroids or anticoags
-you can to avoid unnecessary treatments if you give diuretics for HF to someone who really has lung problems then it could make them worse
helps with early intervention , monitoring
reduced cost with decreased hospitalizations, prevents complications
