Ejection fraction - blood ejected from the heart - normal = 65-80% - max = 85%

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

Cardiac Flashcards by Ben Holtom

What is Heart Failure

inadequate cardiac output to meet the demands of peripheral muscle

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Evaluation of Cardiac Function

ECHO
Pressure/Pressure-Volume
- in vitro
- in vivo
Histology

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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

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CO is greatest affected by?

Heart rate

- stroke volume doesn’t change much

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Fractal shortening

= (EDD-ESD) / EDD

shortens 35-45%

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Ejection fraction

blood ejected from the heart
normal = 65-80%
max = 85%

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Echo

- increase size of heart (LV) will….

decrease ejection fraction %

- does not mean dysfunction

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EDD and ESD

End diastolic/systolic dimension

- echo

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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

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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!!

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Healthy state hypotrophy

pregnancy

athlete

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Purpose of posterior wall thickness? how to find?

Decrease may indicate infarction

posterior wall during diastole
(where fluid stops and starts

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how is EF (% volume ejected by heart) estimated?

LV cone shaped

- calculate base to measure the volume change of the cone

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ECHO information

more structure than function

Heart size - EDD
- once you know size of base can calculate

function/dysfunction
- FS and EF

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Classification of heart failure

- what symptoms to consider

vary during rest and activity (Class 1-4)

fatigue
palpitation
dyspnea (laboured breathing) during activity

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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)

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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….

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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

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broken heart syndrome?

takotsubo

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stroke volume

70ml/beat

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beats per minute

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