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Z YEAR 2 BRS CARDIO > Structural Heart Disease > Flashcards

Structural Heart Disease Flashcards

1
Q

where does blood go during diastole?

A

cardiac chambers start to fill with blood

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2
Q

what happens during the atrial kick? (4)

A
  1. atrial depolarisation

  2. atria contracts

  3. bump in atrial pressure

  4. final push of blood into ventricles before ventricles start to depolarise at AVN
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3
Q

what happens following depolarisation? (spike on ECG)

A
  1. ventricles contract

  2. back-flow of blood causes AV valves (mitral L and tricuspid R) to shut

  3. now both mitral/tricuspid and aorta/pulmonary valves are shut

  4. so volume stays constant and pressure increases

  5. massive pressure increase, needed so ventricular pressure is higher than aortic

  6. causes aortic valve to open, blood reaches rest of body (or lungs for pulmonary)
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4
Q

what happens during repolarisation? (ST segment)

A
  1. ventricles relax so pressure is lower in ventricles than in the aorta

  2. backflow into ventricle from aorta/pulmonary artery, causes respective valve to shut

  3. volume stays constant and chamber relaxes so pressure falls rapidly

  4. pressure in ventricles is lower than in atrium so mitral or tricuspid valve opens

  5. passive filling of ventricles, cycle starts again

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5
Q

which phase gets impaired first in pathological states? (e.g. heart failure)

A

isovolumetric relaxation phase impaired first

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6
Q

why is it important to treat this phase?

A
  1. administer beta blockers as early as possible to minimise damage to the heart
    2, coronary arteries supply myocardium so this phase is important
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7
Q

what is preload?

A

wall stress / force applied to unit cross sectional area of myocardium in diastole

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8
Q

what is preload determined by?

A
  1. Starling’s law of the heart

2. cardiac contractility

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9
Q

describe Starling’s Law

A

Starling’s Law: length-tension relationship
stretch of myocardium in diastole enhances contractile energy generated by this muscle
ascending portion of this relationship is where myocardial contraction should be to produce max contraction


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10
Q

what two factors determine this relationship?

A
  1. immediate effect - not to do with intracellular calcium or any other energy source
→ stressing myocardium reduces overlap of myocardial fibres, decreases interference causing negative effects on contractile energy

  2. slower effect - sub-cellular increase in calcium stores
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11
Q

What is the Anrep effect?

A

increases force of contraction by increasing number of cross bridges formed in myocardium

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12
Q

name the two factors that determine cardiac contractility

A
  1. sympathetic tone - sympathetic nerve fibres supplying myocardium

  2. adrenaline - increasing contractile force of myocardium
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13
Q

how is preload involved in some pathological states (e.g. hypovolemia)?

A
  1. patient bleeding or dehydrated, less energy of contraction (less preload)

  2. less stretching of myocardium to generate contractile force

  3. b.p. falls, stroke volume decreases and energy of contraction decreases
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14
Q

What is afterload?

A
  1. pressure in aorta, force per unit cross section area


2. opposes shortening of myocardium in isotonic manner

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15
Q

how is afterload involved in hypertension?

A
  1. increased afterload impairs stroke volume

2. 
adverse effects such as negative remodelling - heart muscle thickens and pumps dysfunctionally

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16
Q

what is La Place’s Law?

A
  • translates internal diameter radius of a chamber to wall tension and internal pressure generated inside the chamber
1. internal pressure generated inside a chamber is directly proportional to wall tension

    2. inversely proportional to radius of chamber
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17
Q

what happens in pathological states? (heart failure / dilated cardiomyopathy)

A
  • radius of chamber increases
1. chamber is unable to generate effective internal pressure

    2. contractility falls

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18
Q

what are the two equations?

A

P=2T/r but also P=2Sw/r
relationship between wall tension and radius has x2 due to 2 curvatures in the heart
Sw is wall stress x wall thickness instead of T for tension

  1. demonstrate relationship between wall stress and wall thickness and internal pressure generated inside chamber

  2. thickness increasing, pressure generated increases
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19
Q

how does La Place’s Law explain the change in athletic hearts?

A
  1. muscle strengthened to increase contractile force to maintain b.p. needed
  2. chamber with small radius, bigger internal force due to wall tension
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20
Q

what happens in a heart with dilated dysfunctional ventricle?

A

conversion of wall tension into internal pressure is not as effective

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21
Q

what happens when the mitral valve opens?

A

left ventricle fills passively from left atrium, eventually pressure in left ventricle greater than atrium → mitral valve closes

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22
Q

what happens when both aortic and mitral valves are shut?

A
  1. rapid increase in ventricular pressure, volume stays constant

  2. increases pressure in aorta, aortic valve opens and blood flows up
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23
Q

what is the straight line and what makes it steeper?

A
  • straight line is contractility index:
    1. sympathetic stimulation causes contractility index to increase to a steeper line (and leftward shift of the curve, height and diameter of curve increases)

    2. shows increase in stroke work generated is due to sympathetic drive
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24
Q

what are the two possible valvular lesions?

A
  1. stenotic lesions: narrowings
2. dilatations: regurgitation lesions
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25
Q

which sided lesion and which valve’s lesion is worst?

A

left sided valvular lesions are more clinically significant
mitral stenosis, aortic stenosis


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26
Q

When is aortic stenosis severe?

A

severe when valve area is <1cm^2

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27
Q

How do you calculate aortic stenosis severity?

A

trans thoracic echocardiogram: calculate severity by determining speed of blood flow through the valve - severe if greater than 4m/s

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28
Q

What are the causes of aortic stenosis?

A
  1. bicuspid aortic valve - in young patients, born with it

  2. elderly patients: degeneration of the valve
rheumatic heart disease
  3. rare: infective endocarditis, hyperuracaemia
29
Q

How is aortic stenosis detected?

A

heart murmur during systole

30
Q

How common is mitral stenosis?

A

less common than aortic stenosis

31
Q

What are the causes of mitral stenosis?

A
  1. rheumatic fever

  2. congenital
  3. 
rheumatoid arthritis

  4. SLE
  5. 
Whipple’s disease
32
Q

What are the long term effects of mitral stenosis?

A
  1. increased pressure in left atrium

  2. increased strain, it dilates

  3. proarrhythmogenic
33
Q

How is mitral stenosis detected?

A

heard during diastole, trickier to recognise

34
Q

What happens when both stenosis are on the left side?

A
  1. increased afterload on left ventricle, has to work harder to pump blood

  2. contraction is less effective

  3. abnormal remodelling

  4. left ventricular hypertrophy
35
Q

What causes mitral regurgitation?

A
  1. rheumatic fever
  2. mitral valve prolapse
  3. infective endocarditis
  4. if LV dilates too much → leaking of valve
36
Q

What are the immediate effects of mitral regurgitation?

A

→ regurgitation of blood when LV contracts

→ less cardiac output

→ less blood being pumped out of aorta, less volume of blood reaching body


37
Q

Why is it important to treat mitral regurgitation?

A

can die of heart failure, become congested → appropriate medication, diuretics
important to treat and replace valve when severe

38
Q

How is mitral regurgitation detected?

A

systolic murmur

39
Q

What are the causes of aortic regurgitation?

A
  1. bicuspid aortic valve
  2. Marfan syndrome
  3. rheumatic fever
  4. high b.p.
  5. infective endocarditis (acute)
40
Q

What happens when aortic regurgitation is severe?

A
  1. blood reaching aorta doesn’t all reach rest of the body

  2. flows back into left ventricle

  3. volume overload in L.V.

  4. it dilates and becomes more inefficient (La Place’s Law)

41
Q

When does the valve need to be replaced in aortic regurgitation?

A

replace valve when symptoms of heart failure
→ fluid in lungs or legs

42
Q

How is aortic regurgitation detected?

A

diastolic murmur

43
Q

what is the clinical significance of cardiac hypertrophy?

A

high risk of mortality, important to diagnose

44
Q

who needs to be screened?

A

screen first degree relatives

45
Q

what are some characteristics you may see?

A
  1. may have abnormal ECG, left ventricles abnormally thickened
may have abnormal thickening in wall in between chambers

  2. can obstruct blood flow through the aorta
  3. murmur can mimic aortic stenosis, heard in systole ‘ejection systolic murmur’

46
Q

What are the problems with a dilated heart?

A

poor contractility (La Place)

47
Q

What can cause this?

A
  1. stress induced
  2. infectious causes
  3. peripartum
  4. sarcoidosis
  5. immune diseases
  6. ischaemic etiology
    → important to do angiogram to diagnose cause and manage patient
family screening also important
48
Q

what is arrhythmogenic right ventricular cardiomyopathy?

A

a group of disorders
can lead to abnormal ventricular arrhythmia → abnormal contraction, impaired cardiac output

49
Q

what does infiltration of fat in ventricles cause?

A
  1. abnormal diameter and function, dilated,

  2. not pumping effectively, can also affect left ventricle (intrinsically linked)

  3. may not be symptomatic

  4. can cause ventricular tachycardia / lead to sudden cardiac death
(check if there is family history of this)
50
Q

what happens to valve stenosis or regurgitation in the long term?

A

eventually progresses and affects the heart → heart failure
patients become fluid overloaded, fluid in lungs or legs


51
Q

why is it important to recognise heart failure?

A
  1. abnormal heart rhythms / death


2. prognosis in heart failure is worse than cancer, important to prevent

52
Q

how are valve lesions detected then treated?

A
  1. transthoracic echocardiography

2. then treat appropriately
replace valve before patient becomes symptomatic or before heart decompensates

53
Q

evaluate the use of metallic valve replacements

A
  1. used to use metallic valve replacements in younger population

  2. ensures durability (lifetime of prosthetic biological heart valve is ~20 years)
  3. don’t want open stenotomy operations (huge scarring, complications each time)
54
Q

What do you need to be on with metallic valve?

A

warfarin (also has complications, difficult to monitor)
interacts with numerous medication and even food
prosthetic valves, increasing emphasis

55
Q

when is trans aortic valve implantation (TAVI) used?

A

used to be for more frail patients who cannot undergo open heart surgery


  1. now benefits low risk patients, using catheters without open heart surgery

  2. less hospital stay, less likely to get other infections (pneumonia), improves mortality
56
Q

why is mitral valve replacement not ideal? what is preferred?

A
  1. more complicated due to arrangement

  2. withstands less added pressure, not easy to replace, rather repair
  3. 
mitral clip: clipped together to improve function, not open heart surgery
57
Q

What is cardiogenic shock?

A
  1. impairment of cardiac systolic function resulting in reduced cardiac output

  2. end organ dysfunction (not getting vital blood supply from stroke volume of heart)
receiving less oxygen and glucose for sufficient aerobic respiration
81% due to MI (STEMI)
58
Q

how is treatment different to other types of shock (septic, neurogenic, hypovolemic etc)?

A
  1. dangerous to give more fluids because chambers cannot pump blood

  2. will increase diameter of ventricles
would decrease contractility (La Place’s Law) patients may decompensate
keep transthoracic echocardiogram at bedside to see if ventricles are not pumping
early coronary angiography to visualise narrow vessels
urgent PCI - percutaneous coronary intervention

  3. stents to open up narrow arteries causing the MI, or urgent coronary artery bypass grafting
59
Q

why do you need to monitor all body systems?

A

due to so much muscle loss they may still be in cardiogenic shock before or after treatment

60
Q

which treatments are available in intensive care?

A
  1. inotropes


2. advanced mechanical support - when ionotropic drugs aren’t effective

61
Q

how do inotropes work? give some disadvantages

A
  1. acts like sympathetic stimulation (on PV loop)
dopamine etc, augments PV loop

  2. also augmentation in end diastolic volume (curve wider in both directions)
  3. 
increase in stroke work and stroke volume

  4. disadvantages - increased risk of arrhythmias, recent MI,
given upon anaphylactic shock, has side effects - due to ongoing necrosis of muscle

62
Q

what are advantages of IABP?

A
  1. more common, don’t need tertiary centre,

2. reduces afterload, augments diastolic pressure in aorta, improves coronary blood flow

63
Q

what does an impella device do?

A
  1. augments systemic blood pressure and increases coronary blood flow

  2. minimises time of ischaemia by improving blood flow during diastole where myocardium is being perfused

64
Q

how do tandem heart device and VA-ECMO work?

A
  1. tandem heart device reduces preload
  2. augments systemic b.p. improving perfusion of myocardium

  3. .VA-ECMO (venoarterial extracorporeal membrane oxygenation)

  4. improves mean b.p. and oxygenation in circuit
only available in tertiary centres
65
Q

what are some complications of these devices?

A

some are easy to insert some need specialist input in specialist tertiary centre
contraindications: already having a pre-existing cardiac disease

66
Q

which devices should not be used when aortic regurgitation?

A

not good to use IABP or impella, augments diastole where there is bloodflow

67
Q

why do you need to monitor with regular blood tests?

A
  • risk of bleeding because it is anti-coagulated

  • VAECMO has its own blood tests, fibrinogen degradation products, make sure circuit is not blocked, may need to change after 2 weeks
68
Q

are these devices permanent?

A
  1. need plan to wean them off the device

2. 
discuss at every ward round, only a temporary measure
may be palliated


Z YEAR 2 BRS CARDIO (18 decks)

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