Cardiac Function Flashcards by Kailea Boerste

CAD
CHF
CVD
ACS

CAD - coronary heart disease
CHF - congestive heart failure
CVD - cardiovascular disease
ACS - acute coronary disease

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Describe cardiovascular disease briely

Types?
c
cb
pa
aa

leading cause of death

4types:
CHD
cerebrovascular disease
peripheral arterial disease
Aortic artherosclerotic disease

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What are some ways CVD begins?

May begin at birth or childhood
congenital heart defect or rheumatic fever

some develop overtime into adult

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CHD overview states
an
m
h

angio pectoris (chest pain)
myocardial infarction (MI)
heart failure

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Cerebrovascular disease states

blood supply cut off from brain
stroke/trans ischemic attack (mini)

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Peripheral arterial disease (PAD)

blockage in arteries
PAD/DVTs

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Aortic artherosclerotic
a
d

aneurysms widening of artery
dissection - tears in aorta

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Describe Artherosclerosis
chronic
accum of
veins?

chronic inflammation
accumulation of lipid material in arteries/veins
veins narrow and harden

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Describe Ischemia

lack of blood flow
localized in heart 1/3rd of deaths
can see in early as age 10

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Describe the damage of endothelial walls in artherosclerosis
t
pl
oc/th/ru

turbulent blood flow
plaque formation in cycle/vessle
occlusions/thrombosis/ruptures/ combos

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most common locations of artherosclerosis
plad
plmc
erca

prox. left anterior decending
prox. left main coronary
entire right coronary artery

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When is artherosclerosis symptomatic?

with 75% plaque formation

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Lack of blood supply in heart leads to?

ischemia

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Classic masnifestation of cardiac ischemia/angina/HA
a
s
rad
inc

angina
squeezing of chest/pressure
radiates to left shoulder/neck/arm
increases in intensity

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non classical manifestation of cardiac ischemia

more common in women
nausea/short breath/stabbing pain

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Do normal ECGs rule out presents of ACS?

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Eval of chest pain
physical exam:

chest xray

physical. exam: high BP cardiac valv disease
ECG chest xray

Chest xray - non cardiac source

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Initial markers of cardiac damage explained

cell death releases..

r
s
d

cell death releases intracellular proteins from myocardium into circulation

1.) released rapidly/steady
2.) several day persistance
3.) detected at low levels

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T/F if STEMI is an issue, do the EKG within 10 min

true

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First cardiac markers
a/l
ck

AST/LD (non specific)

creatinine kinase in nearly all cells

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CK isoenzymes

whats most reliable indicator of MI?

CK MB most reliable

CK-MM muscle

CK-BB brain

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What other disease states can CK-MB be elevated in?

can be elevated in chronic muscle disease, end stage renal and intense excersise

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What do troponin levels look like if the myocardium is undamaged?

normal

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Cardiac troponins
complex of…

TnT
TnI
TnC

complex of 3 proteins, transmit calcium signals to contract muscles

TnT - binds to tropomycin
TnI - inhibits binding of actin/myosin
TnC - binds to calcium to reverse TnI

Briefly describe tissue specific isoforms

slow/fast cardiac muscles

CTnc same..

same isoform for both slow twitch (T2) and cardiac

CTnI-CTnT unique

unique isoforms in fast twitch/slow and cardiac

T/F each isoform is encoded in separate genes

true

What is CTnI specific forc detection of .... in how many hours after onset? lasts? widest window for detection post.. high?

cardiac injury detection of myocardial cell injury acute ischemia/myocard 3-12 hr after onset/for weeks widest window for detection post MI and high sensitivity/specificity

Specificity/sensitiv of troponin what kind of release?

slow release may not be detected when pt presents with early pain rise and fall of troponin indicate AMI

HS-CTn confirms....at low [] discerns ...associated with

can confirm myocardial injury at low concentration discern small changes in {} delta values associated w probability of risks

Challenges of troponin chronic un single rule other diseases unstb struct arth

chronic unhealthy people w chest pain single rule out value due to high sensitivity procedures and other diseases : unstable angina struct HD arhterosclerosis

Pts with kidney disease prognosis in CKD increases? predicts? dialysis elevation of? increases? hemodyalisis involves filt?

prognosis in CKD increase troponin levels predict worse long term cardiac issues dialysis elev in CTnT increase mortality hemodylsis involves filt of blood of toxins diff concent of enzymes

Myoglobin what type of binding released? spcificity/half life? used with?

iron oxy bind in muscles small protein released when muscles damages not specific short half life used along w CK-MB and troponin

HS-Tn can detect before?

myoglobin

Cardiac injury occurs in? what happens? cells removed by? when energy fails? reperfusion transfusions?

occurs in MI = cell death apoptosis or necrosis apoptic cells removed by macrophages - requires energy (necorsis when enrgy fails) Reperfusion transfusions: intravasc baloons, CABG/chem thrombosis

Biomarkers in heart failure descirbe heart failure manifestations

heart failure: pathological condition when heart fails to inadequatly supply metabolic needs of body, decreases pumping manifest: retention of fluids, shortness of breath, lower extremity edema

Reccommendations of heart failure markers

CTnI, CTnT, excersise stress test, X-ray

Diagnosis and risk stratification of heart failure most common presence of heart failure sympt? what distinguishes cardiac vs non cardiac dspnea what is secreted in response to inc pressure/load on heart?

shortness of breath most common presense of heart failure - very non specific BNP or precursor NT-proBNP cardiac/non cardiac dyspnea naturetic peptides secret from heart in response to incr pressure/volume load

Reducing intravasc volume steps promote n/d/v inhibit sns

promote natr/diu/vasodilation inhibit sympathetic nervous system signalling

BNP/NT-ProBNP released from ..... in response to in what kind of pts predicts?

released from myocardial cells in response to incr vol/incr pressure/hypertrophy Both in pts with ventricular dysfunction strong predic mortality

BNP/NT-ProBNP continued what is the same? optimal? what is being persued as target?

sensit/spec are same - optimal cut off vals BNP being persued as target by manufacutures

Cardiac troponins diagnosis of who else has elevations ongoing.. impaired?

diagn of Myocardial injury heart failure pts have elev as well as ongoing cell death impaired liver

Detection of heart failure

not diagnostic, stratify risk/prognosis concomintant elev in multiple markers associated w esclating risk of effects

Is CTnI or CTnT more common in heart failure

CTnI

markers of CHD and plaque instability m/c indicate presnce of... predict provide progn from...

MPO and CRP may indicate presence of inflam to predict mortality and provide progn from clinical risk and Hs-CTnT

MPO increased in ...a/c

released when neuts gather in blood vessles increased in ACS and chronic CAD

CRP

marker of inflammation HS-CRP progn marker of artherosclerosis/CHD <1mg normally

Lipoprotein A predicts prem..

predict premature cardiovasc disease

Homocystine what kind of AA how many forms? total plasma HC refers to? normal levels? linked with? inc risk with

sulfur containing AA 4 forms total plasma HC refers to all 4 forms norm 5-15 linked w high levels and CVD inc risk with elevation

hyperhomocystemia risk factor of? inc 5 mol =

CVD <40% pts w CVD have hyperhomo increase 5mol = HD inc 20-30%

Pulmonary embolism embolous puml embolism extent?

embolous - mass of solid/liq/gas pulm embolous: high risk lodged in pulm arteries impares flow size and location affect extent

Saddle emboli lodged at bif... inc h inc incidence w whos at higher risk?

lodged at bifuracation of main artery, blocks pulm blood flow increase heart failure incidence inc w age women at higher risk

Use of D dimer when pretest prob... cross indicated coag.. high

when pretest prob of PE is low cross linked fibrin indicates coag indirect marker/fibrinolysis high sensitivty/quant

Abn levels of D dimer

90% of pts with PE pts w normal levels rule out PE

Troponin and PE progn val w short term? clinic agr

progn val w PE short term mortality clinical management agression

BNP with PE evals ... neg pred values? IDs pts with...

elev vals inc short term mortality 94% neg pred values ID pts w acute PE and high risk adverse outcomes

CHD w PE common? can cause?

uncommon substantial mortality arhterosclerosis can cause ischemia