Cardiac Flashcards
What is Heart Failure
inadequate cardiac output to meet the demands of peripheral muscle
Evaluation of Cardiac Function
- ECHO
- Pressure/Pressure-Volume
- in vitro
- in vivo - Histology
ECHO
echocardiogram
- sound wave bounces through heart to see structures in cross section (long and short axis)
left side - cone shaped
right side - hard to see because of lung (fluid filled - bounces in all directions
CO is greatest affected by?
Heart rate
- stroke volume doesn’t change much
FS
Fractal shortening
= (EDD-ESD) / EDD
shortens 35-45%
EF
Ejection fraction
- blood ejected from the heart
- normal = 65-80%
- max = 85%
Echo
- increase size of heart (LV) will….
decrease ejection fraction %
- does not mean dysfunction
EDD and ESD
End diastolic/systolic dimension
- echo
Limitation of measuring EF of echo?
assumption that cone shape in normal heart stays the same during disease state (NOT true)
athletes - increase heart size–> decrease EF
same SV and CO
Parameter of ECHO that may suggest heart failure?
Fractal Shortening = (EDD-ESD) / EDD
ex. cTAC continous transverse aortic constriction (forced hypertension)
- causes decrease in FS
NOT YET HF!!
Healthy state hypotrophy
pregnancy
athlete
Purpose of posterior wall thickness? how to find?
Decrease may indicate infarction
- posterior wall during diastole
(where fluid stops and starts
how is EF (% volume ejected by heart) estimated?
LV cone shaped
- calculate base to measure the volume change of the cone
ECHO information
more structure than function
Heart size - EDD
- once you know size of base can calculate
function/dysfunction
- FS and EF
Classification of heart failure
- what symptoms to consider
- vary during rest and activity (Class 1-4)
fatigue
palpitation
dyspnea (laboured breathing) during activity
Classification of heart failure
- classes based on exercise intolerance
Limitations
I - none (risk factors only)
II - slight limitation (during ordinary activity, comfortable at rest
III - marked (less than ordinary, comfortable at rest)
IV - Unable (insufficient at rest)
Why care about EF is we have FS?
closely linked - similar data
lower FS should mean lower EF
- EF decrease with increase size
-consider other variables….
Why study drosophila
unable to phenotype the human heart
- TNI mutant gene seen in flies is found to cause myopathy in humans
- normally able to have 100% FS but with mutant its reduced
broken heart syndrome?
takotsubo
stroke volume
70ml/beat
beats per minute
72
initial events of CHF
arrythmeias HCM diabetes DCM Ischemia Hypertension CAD
The heart moves…
oxygen
heat
waste products
communication
p wave problem
atrial hypertrophy
right - large p wave
left - two humped p wave
why have purkinje
ventricles contract diff time
Channelopathies cause? symptoms?
Long QT syndrome
- fainting
- seizures
- sudden death
Sodium channel channelopathy
brugada syndrome
blood clot in auricle
atrial thrombus
- veins or damaged arteries
treatment of blood clots? problem?
blood thinners (TPA, warfrin, aspirin) - no blood flow to brain, must wait for diffusion
atrial fibrillation
arrythmea
- ventricles contract faster than normal
- rotors
- spontaneous depol on av
3 types
- paroxysmal
- persistent
- permenant
Triggers for AF
increase body fluid
- outside body
- SVC IVC hypertension, demand more work
remodelling from AF
fibrosis fat CHO less caps connexin 40 (gap junctions) less cardiomyocites
AF treatment
anti arrhythmic drugs
- toxic and make it worse
cardiac ablation
-kill rotors, isolate rotors # cuts
Fish oil
-with 30min decrease development
Corticosteriods
- decrease inflammation from dying cells
- decrease trigger sensativity
INR
international normalized ratio
- rate at which it takes blood to clot
- increase too high will increase intracranial bleeding
Av blocks
1st degree
- prolonged P-QRS
2nd
-2 P waves per QRS
3rd
-2:1 but not P driven
Overstimulated HR
ventricular tachychardia
Ventricular Fibrilation
no pattern of heart beat on ECG
ST elevation
STEMI
completely blocked coronary art
- severe Heart attack
only 50%, could be LBBB of LVH
picks up on 45% of stemi
Angina
symptom of low O2
CAD
lactic acid causes pain
Ischemia
low –> no blood flow
angina types
predictable (duration and intensity)
unstable (more severe, frequent and unstable)
variant (spontaneous - arteriol spasm)
problem with angina when diagnosing heart attack
only 12-18
- could be COPD, gas, stressed muscle, etc
when looking for open/closed arteries
angiograms
- dye plus xray
disease progression
angina
myocardial infarction
heart failure
heart damage
necrosis
biomarker with heart attack
cardiac Troponin 1 or T
treating blockage (athlerosclerosis)
stent
- push up against walls, holds it their
- filled with medication (anti inflammatory)
3 ways to develop a block
- athleroscleoris
- blood clot
- spasm (causes variant angina)
collateral circulation
increase number and size of blood vessels to pass the block
early damage
later damage
subendocardial infarct
- blood flow out to in
- endocardial muscle dies first
transmural infact
- 8 hrs to reach epicardium
