Cardiology Flashcards

1
Q

Function and location of the trabeculae carnea

A

Project from the inner surface of the right and left ventricle.
Provide additional support to ventricular valves, maintaining stroke volume and cardiac output

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2
Q

What do the heart sounds correlate to?

A

S1 - tricuspid and mitral valve shutting
S2- closed aortic and pulmonary valve
S3 – linked with flow of blood into the ventricles.
S4 – linked with atrial contraction.

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3
Q

What stages are isovolumetric relaxation and contraction?

A

Relaxation- semilunar valve and atriaventricular valves closed but pressure reducing
Contraction- semilunar valve and atrioventricular valve closed but pressure is increasing

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4
Q

Give 4 congenital heart defects examples and describe them

A

Atrial Septal defect - hole in the wall between both atria
Ventricular septal defect - hole in the wall between both ventricle
Tetralogy of Fallot - overarching aorta over vsd, right pulmonary hypertrophy, ventricular septal defect, narrowing of the pulmonary artery (pulmonary stenosis)
Coarction of the aorta - narrowing of the aorta, leads to thickening of the ventricles

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5
Q

Aortic stenosis:
What is it preceded by?
How is it suspected?
What age is it most likely to happen?
What are the risk factors (8)?
Aetiology
Describe the pathophysiology
What does it lead to?
What happens in rheumatic heart disease?
Presentation(6)?
What do they normally have a history of (5)?
What investigations occur(4)?

A
  1. Aortic sclerosis
  2. Crescendo diminuendo systolic murmur , echo-cardiogram
  3. 60/70s
  4. High LDL, high C-reactive protein level, Radiotherapy, CKD, Older age, Congenital bicuspid valve, hypertension, smoking
  5. Rheumatic heart disease, congenital heart disease, calcium build up
  6. irritation of the endocaridum of the valve, leads to an inflammatory response that leads to deposition of calcium and leaflet fibrosis and therefore narrowing
  7. LVH
  8. Following untreated strep, autoimmune response that leads to inflammatory response and calcium deposition
  9. End systolic murmur, syncope, angina, heart failure, exertional dysponea and fatigue, heart failure
  10. High LDL , CKD, rheumatic fever, high lipoprotein, age >65
  11. TRansthoracic echocardiography , cardiac catherisation, cardiac MRI, ECG chest x-ray
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6
Q

Aortic regurgitation:
What kind of murmur?

What are the congenital and acquired causes (5)?
What are the causes of it through aortic root dilation?
Describe the pathophysiology of acute AR
Describe what happens physiology afterwards
Describe the pathophysiology of chronic AR
Describe what happens physiologically afterwards
How does acute AR present (4)?
How does chronic AR present (2)?
What investigations are done?
What is the management of acute AR?
What is the management of (a)symptomic chronic AR?

A
  1. early diastolic murmur
  2. Congenital heart defect congenital bicuspid valve, infective endocarditis, rheumatic fever, aortic valve stenosis
  3. Marfan’s syndrome, idiopathic, connective tissue disease, trauma, ankylosing spondylitis
  4. Infective endocarditis, trauma, vegetations
  5. Backflow of blood therefore increased end systolic volume and pressure, increased end diastolic LV pressure, increased pulmonary venous pressure, pumonary oedema, dyspnoea, cardiogenic shock, heart failure
  6. Rheumatic fever, congenital bicuspid valve
  7. Left ventricular enlargement and eccentric hypertrophy, initially ejection fraction okay but eventually it reduces and end systolic pressure increases eventually LV dyspnea, lower coronary perfusion, ischaemia. necrosis and apoptosis , heart failure
  8. Pulmonary oedema, tachycardia, cardiogeic shock, blue tinged lips - cyanosis
  9. Wild pulse pressure, pistol shot pulse (Traube sign)
  10. Transthroacic echocardiogram, cardiac catherisation, cardiac mri, ecg chest x ray
  11. Valve replace and treat cardiogenic shock first - vasodilators
  12. a. drugs and reassurance b. avr and vasodilators
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7
Q

Mitral stenosis:
What does it lead to final progression?
What are the main causes (9)?
Describe the pathophysiology
How does this effect physiology?
Presentation (8)
Investigations to carry (5)
Management

A
  1. Pulmonary hypertension and therefore right heart failure
  2. Rheumatic fever, Carcinoid syndrome, SLE, congenital defect of heart, calcification caused by ageing, ergot/serotonergic drugs, rheumatoid arthiritis, whipple disease, amyloidosis
  3. Many years after rheumatic fever, eventually leads to formation of multiple foci and infiltrates the endo and myocardium, gets thickened, calcified and contracted
  4. initially moderate exericse, tachycardia causes dyspnea on exertion, overtime transudation of fluid into lung interstitium so dyspnea at rest, haemoptysis if bronial vein ruptures due to increased pressure, reduced cardiac output pulmonary hypertension,
  5. Mid diastolic murmur, dyspnea, orthodyspnea, heamoptysis, history of rheumatic fever, loud P2, neck vein distension, 40 -50 yrs age
  6. ECG, chest x ray, cardiac MRI, transthoracic echocardiogrma, cardiac catherisation
  7. Asymptomatic leave it alone, severe asymptomatic adjuvant balloon valvotomy, symptomatic adjuvant balloon valvotomoy, diuretics, valve replacement, repair adjunt beta blockers
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8
Q

Mitral regurgitation:
Causes of acute MR (5)
Causes of chronic MR (5)
Describe the pathophysiology
How does this affect heart physiology?
Presentation (7)
Investigation (5)
Management

A
  1. Rheumatic heart disease, Infective endocarditis, mitral valve proplapse, valvular surgery, prosthetic mitral valve dysfunction
  2. Rheumatic heart disease, SLE, Scleroderma, Hypertrophic cardiomyopathy, Drug related
  3. Following infective endocarditis or rheumatic heart disease - leaflet perforation, vegetation along cusps, damage to chordae tendinae, abscess formation and others. Eventually leads to back flow of blood to atrium, this causes increased volume of ventricle during diastole , this leads to lv dilation remodelling leading to reduced LV systolic function, back pressure in left atria and eventually pulmonary congestion, at the same time decreased stroke volume and cardiac output so congestive heart failure
  4. Dilated LV
  5. dyspnoea, holosystolic murmur , S3 sounds, congestive heart failure, peripheral oedema
  6. ECG, transthoracic echocardiogram, chest x ray, cardiac cathrisation, cardiac MRI
  7. Acute MR- straight to surgery, prosthetic ring
    CHronic asymptomatic - watchful waiting
    <60% EF surgery
    CHronic symptomatic - <30 % EF intra aortic balloon counterpulsation
    Firts line surgery + meds
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9
Q

What drugs can be used to manage the symptoms of Dilated cardiomyopathy?

A

Arrythmia- Amiodarone
Heart failure- ACEi, b-blockers
2nd line: ARB, Diuretics

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10
Q

What kind of abnormalities can ECG tell us about?

A
  • Conduction
  • Structural (e.g. ventricular hypertrophy)
  • Perfusion (whether the muscle is ischaemic or infarct e.g. MI)
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11
Q

Deflections in cardiac vectors denotion

A

Steepness of deflection denotes the ‘velocity’ of action potential

Width of the deflection denotes the ‘duration’ of the event

Downward deflections are towards the –ve electrode

Upward deflections are towards the +ve electrode

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12
Q

Describe what each little part of the ECG indicates:
P wave -
Isoelectric line following p wave -
Isoelectric line before Q peak
Q peak
R peak
S peak
Isoelectric line after S
T peak

A

Sino atrial node

Atrioventricular node

Bundle of His

Bundle branches

Ventricular contraction

Late ventricular contraction

Fully depolarised ventricles

Ventricle repolarisation

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13
Q
  • Rule of Ls for limb leads
A

Lead I (1 L) → Right arm to Left arm
Lead II (2 Ls) → Right arm to Left Leg
Lead III (3 Ls) → Left arm to Left Leg

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14
Q

What does aVL read?

A

Compares the electrical activity between a positive electrode on the left arm with the average electrical activity between the right arm and left leg (lead II)

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15
Q

What does aVR read?

A

Compares the electrical activity between a positive electrode on the right arm with the average electrical activity between the left arm and left leg (lead III)

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16
Q

What does aVF read?

A

Compares the electrical activity between a positive electrode on the left leg with the average electrical activity between the right arm and left arm (lead I)

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17
Q

Atrial fibrillations vs atrial flutter

A

Oscillating baseline – atria contracting asynchronously
vs
Regular saw-tooth pattern in baseline (II, III, aVF)

18
Q

First degree heart block features

A

Prolonged PR segment/interval caused by slower AV conduction

Regular rhythm: 1:1 ratio of P-waves to QRS complexes

19
Q

Second degree heart block (Mobitz I) features

A

Gradual prolongation of the PR interval until beat skipped

Most P-waves followed by QRS; but some P-waves are not

Regularly irregular: caused by a diseased AV node

20
Q

Second degree heart block (Mobitz II) features

A

P-waves are regular, but only some are followed by QRS

No P-R prolongation

Regularly irregular: successes to failures (e.g. 2:1) or random

Can rapidly deteriorate into third degree heart block

21
Q

Third degree complete heart block features

A

P-waves are regular, QRS are regular, but no relationship
P waves can be hidden within bigger vectors

22
Q

Ventricular tachycardia features

A

P-waves hidden – dissociated atrial rhythm

Rate is regular and fast (100-200 bpm)

23
Q

Ventricular fibrillations

A

Heart rate irregular and 250 bpm and above

Heart unable to generate an output

24
Q

ST elevation features

A

P waves visible and always followed by QRS (1:1)

Rhythm is regular and rate is normal (85 bpm)

ST-segment is elevated >2mm above the isoelectric line

Caused by infarction (tissue death caused by hypoperfusion)

25
Q

What three tests are invoolved in the exercise capacity test?

A

Cardiopulmonary exercise test

Six minute walk test

Incremental shuttle walk test

26
Q

Cardiopulmonary exercise test
What is involved?
What is routinely measured?
Outputs?
Advantages and Disadvantages

A
  1. Uses a cycle ergometer or treadmill
    Intensity is incremental
    Undertaken under close clinical supervision in a controlled environment
  2. ECG, ventilation, O2 and CO2 routinely measured
  3. Peak VO2 is usually the primary outcome
  4. Advantages:
    - Quantifies performance in relation to metabolism
    - Precise and reproducible
    - Continuous monitoring for safety

Disadvantages:
- Requires skilled technical support (calibration and
- Very expensive (initial & ongoing costs)
- Needs dedicated space

27
Q

Six minute walk test:
What is involved?
Outputs
Advantages and Disadvantages

A
  1. Uses a 20-30 m flat course (e.g. corridor)
    Objective is to cover greatest distance as possible in six minutes
    Externally timed by assessor
    Sub-maximal test
  2. -A: total distance walked in six minutes
    -B: ‘perceived exertion’ scales, heart rate and pulse oximetry
  3. Advantages:
    Patient-driven pace – speeding up, slowing down & rest OK
    Cheap to deploy
    Validated in many clinical populations

Disadvantages:
Requires a significant unobstructed course, it often undertaken in a public hospital corridor
The pace is not regulated (non reproducible)

28
Q

Incremental shuttle walk test:
What is is involved?
Outputs
Advantages and Disadvantages

A
  1. Uses a 10 m circuit
    Externally paced by an audio recording (like bleep test)
    Each minute has one extra length than the previous minute

2.
A: is total distance walked before you choose to end
B: ‘perceived exertion’ scales, heart rate and pulse oximetry

  1. Advantages:
    Cheap to deploy
    Validated in many clinical populations
    The external pacing helps some to achieve maximum levels

Disadvantage:
- Requires an unobstructed course, it is often undertaken in a public hospital corridor
- For some the incremental nature is difficult (min. speed 1.8km/hour)
-Patient can be penalised for poor pace management

29
Q

Risks factors for coronary heart disease

A

Modifiable factors:
1.smoking, lipids intake, blood pressure, diabetes,obesity, sedentary lifestyle
Non-modifiable factors:
1- age, sex, genetic background

30
Q

Main cell types involved and their roles in atherosclerosis

A

Vascular endothelial cells
Platelets
Monocyte - Macrophage
Vascular smooth muscle cells
T lymphocytes

31
Q

In what ways do macrophages affect atherosclerosis?

A

Inflammatory macrophages - Adapted to kill microorganisms

Non inflammatory macrophages and Resident macrophages - normally homeostatic function, alveolar resident macrophages , spleen - iron homeostasis

32
Q

Modification of subendothelial trapped LDL in atherosclerosis

A
  1. LDL leak through the endothelial barrier
  2. Trapped by binding to sticky matrix carbohydrates in the subendothelial layer and becomes susceptible to modification
  3. Best studied modification is oxidation - free radical attack from activated macrophages
  4. LDL becomes oxidatively modified by free radicals from activated macrophages
  5. Oxidised LDL is phagocytosed by macrophages and stimulate chronic inflammation
33
Q

Familial hyperlipidemia description

A

Autosomal genetic disease
Massively elevated cholesterol
Failure to clear LDL from blood

34
Q

Scavenger receptor description

A

A family of pathogen receptors that accidentally bind OxLDL

Macrophages scavenger receptor A & B
Receptor A:
Known as CD204
Binds to oxidised LDL
Binds to gram positive bacteria like staphylococcus&streptococcus
Binds to dead cells

Macrophage scavenger receptor B:
Known as CD36
Binds to oxidised LDL
Binds to malaria parasites
Binds to dead cells

35
Q

What is the pharmacological functional name of statins?

A

HMG - CoA reductase inhibitors

36
Q

Importance of LDL receptor PCSK9 inhibitors

A

PCSK9 degrades LDLRs
Now used to supplement statins

37
Q

What are the cholesterol export pumps?

A

ABCA1/ ABCG1

38
Q

What enzymes from macrophages further oxidise LDL?

A

NADPH oxidase
Myeloperoxidase
Generation of H2O2

39
Q

Macrophage with plaque formation

A

Generate free radicals that further oxidise lipoproteins

Phagocytose modified lipoproteins and become foam cells

Express cytokines mediators that recruit monocytes ( positive feedback loop)

Express attractants and growth factor for VSMC ( vascular smooth muscle cells)

Express proteinases that degrade tissue

40
Q

What

A