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CardioResp Phys HK4550 > Cardiac > Flashcards

Cardiac Flashcards

1
Q

What is Heart Failure

A

inadequate cardiac output to meet the demands of peripheral muscle

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2
Q

Evaluation of Cardiac Function

A
  1. ECHO
  2. Pressure/Pressure-Volume
    - in vitro
    - in vivo
  3. Histology
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3
Q

ECHO

A

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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4
Q

CO is greatest affected by?

A

Heart rate

- stroke volume doesn’t change much

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5
Q

FS

A

Fractal shortening

= (EDD-ESD) / EDD

shortens 35-45%

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6
Q

EF

A

Ejection fraction

  • blood ejected from the heart
  • normal = 65-80%
  • max = 85%
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7
Q

Echo

- increase size of heart (LV) will….

A

decrease ejection fraction %

- does not mean dysfunction

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8
Q

EDD and ESD

A

End diastolic/systolic dimension

- echo

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9
Q

Limitation of measuring EF of echo?

A

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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10
Q

Parameter of ECHO that may suggest heart failure?

A

Fractal Shortening = (EDD-ESD) / EDD

ex. cTAC continous transverse aortic constriction (forced hypertension)
- causes decrease in FS

NOT YET HF!!

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11
Q

Healthy state hypotrophy

A

pregnancy

athlete

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12
Q

Purpose of posterior wall thickness? how to find?

A

Decrease may indicate infarction

  • posterior wall during diastole
    (where fluid stops and starts
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13
Q

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

A

LV cone shaped

- calculate base to measure the volume change of the cone

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14
Q

ECHO information

A

more structure than function

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

function/dysfunction
- FS and EF

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15
Q

Classification of heart failure

- what symptoms to consider

A
  • vary during rest and activity (Class 1-4)

fatigue
palpitation
dyspnea (laboured breathing) during activity

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16
Q

Classification of heart failure

- classes based on exercise intolerance

A

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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17
Q

Why care about EF is we have FS?

A

closely linked - similar data

lower FS should mean lower EF
- EF decrease with increase size

-consider other variables….

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18
Q

Why study drosophila

A

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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19
Q

broken heart syndrome?

A

takotsubo

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20
Q

stroke volume

A

70ml/beat

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21
Q

beats per minute

A

72

22
Q

initial events of CHF

A 
arrythmeias 
HCM
diabetes
DCM
Ischemia
Hypertension
CAD
23
Q

The heart moves…

A

oxygen
heat
waste products
communication

24
Q

p wave problem

A

atrial hypertrophy
right - large p wave
left - two humped p wave

25
Q

why have purkinje

A

ventricles contract diff time

26
Q

Channelopathies cause? symptoms?

A

Long QT syndrome

  • fainting
  • seizures
  • sudden death
27
Q

Sodium channel channelopathy

A

brugada syndrome

28
Q

blood clot in auricle

A

atrial thrombus

- veins or damaged arteries

29
Q

treatment of blood clots? problem?

A 
blood thinners (TPA, warfrin, aspirin)
- no blood flow to brain, must wait for diffusion
30
Q

atrial fibrillation

A

arrythmea

  • ventricles contract faster than normal
  • rotors
  • spontaneous depol on av

3 types

  • paroxysmal
  • persistent
  • permenant
31
Q

Triggers for AF

A

increase body fluid

  • outside body
  • SVC IVC hypertension, demand more work
32
Q

remodelling from AF

A 
fibrosis
fat
CHO
less caps
connexin 40 (gap junctions)
less cardiomyocites
33
Q

AF treatment

A

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
34
Q

INR

A

international normalized ratio

  • rate at which it takes blood to clot
  • increase too high will increase intracranial bleeding
35
Q

Av blocks

A

1st degree
- prolonged P-QRS

2nd
-2 P waves per QRS

3rd
-2:1 but not P driven

36
Q

Overstimulated HR

A

ventricular tachychardia

37
Q

Ventricular Fibrilation

A

no pattern of heart beat on ECG

38
Q

ST elevation

A

STEMI
completely blocked coronary art
- severe Heart attack

only 50%, could be LBBB of LVH
picks up on 45% of stemi

39
Q

Angina

A

symptom of low O2
CAD
lactic acid causes pain

40
Q

Ischemia

A

low –> no blood flow

41
Q

angina types

A

predictable (duration and intensity)
unstable (more severe, frequent and unstable)
variant (spontaneous - arteriol spasm)

42
Q

problem with angina when diagnosing heart attack

A

only 12-18

- could be COPD, gas, stressed muscle, etc

43
Q

when looking for open/closed arteries

A

angiograms

- dye plus xray

44
Q

disease progression

A

angina
myocardial infarction
heart failure

45
Q

heart damage

A

necrosis

46
Q

biomarker with heart attack

A

cardiac Troponin 1 or T

47
Q

treating blockage (athlerosclerosis)

A

stent

  • push up against walls, holds it their
  • filled with medication (anti inflammatory)
48
Q

3 ways to develop a block

A
  • athleroscleoris
    • blood clot
  • spasm (causes variant angina)
49
Q

collateral circulation

A

increase number and size of blood vessels to pass the block

50
Q

early damage

later damage

A

subendocardial infarct

  • blood flow out to in
  • endocardial muscle dies first

transmural infact
- 8 hrs to reach epicardium

CardioResp Phys HK4550 (5 decks)

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