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FINALS > CARDIOLOGY > Flashcards

CARDIOLOGY Flashcards

1
Q

How is heart failure classified?

A

Left or right sided
Congestive

Systolic: insufficient contraction (reduced ejection fraction v. Diastolic insufficient relaxation therefore insufficient filling (preserved ejection fraction)

Acute v chronic

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2
Q

What are the causes of left heart failure?

A

Ventricular inflow obstruction (blood can’t flow into ventricles)

Diastolic dysfunction
(not enough blood flows in)

Reduced ventricular contractility (doesn’t contract as well)

Ventricular volume overload
(too much blood flows in)

Ventricular outflow obstruction
(blood can’t flow out)

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3
Q

What causes ventricular inflow obstruction? (blood can’t flow into ventricles)

A

The atrial-ventricular valves not functioning:

Mentral valve or Tricuspid valve stenosis

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4
Q

What causes diastolic dysfunction? (heart doesn’t fill enough)

A

Constrictive pericarditis

Cardiac tamponade

Arrhythmias

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5
Q

What causes reduced ventricular contractility?

A

MI

CAD

Dilated cardiomyopathy

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6
Q

What causes ventricular volume overload? (too much blood flows in)

A

Mitral regurgitation

VSD and ASD

Increased metabolic demand for blood

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7
Q

What causes ventricular outflow obstruction? (Blood can’t flow out)

A

Aortic stenosis

Pulmonary stenosis

Pulmonary hypertension

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8
Q

What are the causes of right heart failure?

A

Left heart failure

Right sided infarct

Congenital heart defect

Pulmonary hypertension and chronic lung disease (e.g. in COPD)

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9
Q

What are the symptoms of left heart failure?

A

Pulmonary (L=lungs) blood backs up in the lungs as it can’t enter the heart, pressure increases and fluid is forced out of the capillaries under pressure causing:
Cyanosis
Tachypnoea
Paroxysmal nocturnal dyspnoea that wakes patient
Bibasal crepitation

Cardiac symptoms are down to the causes
Murmurs
Laterally displaced apex beat

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10
Q

What are the symptoms of right heart failure?

A 
Blood backs up trying to get into the right heart forcing fluid out of the capillaries under pressure resulting in:
Ascites
Peripheral pitting oedema 
Tender hepatomegaly
Parasternal heave 
Riased JVP
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11
Q

What is preload?

A

Volume of blood in the ventricles at the end of diastole = End Diastolic Volume a

This is measured by the pressure it exerts on the ventricle walls

Essentially a measure of the patient’s volume status

Low pre-load = low volume e.g. in shock, hypotension and tamponade

High pre-load = high volume e.g. in heart failure and bradycardia

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12
Q

What is afterload?

A

Pressure the ventricles exert to open the pulmonary/aortic valves which must be greater than the pressure greater by the peripheral vessels (TPR)

After-load is high in: Hypertension (the TPR is higher so more pressure is needed), aortic stenosis (greater pressure is needed to open the valve) and SNS stimulation as that causes increased TPR to redirect blood to needed structures

After-load is low in: Hypotension and sepsis (due to vasodilation)

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13
Q

What is Starling’s law?

A

The more the heart muscle stretches the harder it contracts (to a point)

In heart failure this point is lower

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14
Q

How does heart failure self-perpetuate?

A

Heart failure leads to reduced C.O which leads to reduced BP which activated the RAASystem.

This retains Sodium and Water which increases preload and causes vasoconstriction which increases afterload.

Increased BP increases cardiac work which increases sympathetic activation which leads to increased cardiac contractility

The heart is forced to work harder and thus is damaged and myocytes are lost, this results in worsening of the heart failure

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15
Q

What are is the NYHA classification for heart failure?

A

I - no limitations
II - slight limitation
III - marked limitation
IV - symptoms at rest and no physical activity without discomfort

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16
Q

What are the signs of heart failure on CXR?

A 
Alveolar oedema: 'bat wings'
kerley B lines (interstitial oedema)
Cardiomegaly (s3+4 heart sounds)
Dilatation of apex arteries (blood Diverted to upper lobe)
pleural Effusion
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17
Q

What is BNP?

A

Brain Naturitic Peptide is produced by the LV myocardium in response to strain

> 400 pg/ml

  • LV Hypertrophy
  • Ischaemia
  • Tachycardia
  • RV overload
  • Hypoxaemia-P.E

Also by: sepsis, GFR <60, COPD, Diabetes, >70 y/o, Cirrhosis

< 100 pg/ml

  • Obesity
  • Diuretics
    • Aldosterone antagonists
  • ACEi/A2RB
  • B blockers
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18
Q

How is heart failure treated?

A

ACEi* (Ramipril) + B-Blocker* (start low, go slow) (Bisoprolol, Carvedilol, Nebrilol)

Aldosterone Antagonist* (Spironolactone)/ A2RB (Candestartan, Losartan)/ Hydralazine + Nitrate* (Isosorbide mononitrate) which are Vasodilators

Cardiac resynchronisation therapy (pacing) or a Cardiac Glycoside (Digoxin) especially in AF

Diuretics can be used if in fluid overload (Furosemide or Spiron)

Flu and pneumococcal vaccine

*shown to improve mortality

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19
Q

What is Acute Coronary Syndrome?

A

Acute presentation of ischaemic heart disease (CAD): Reduced blood flow to the heart muscle due to vessel disease

STEMI
NSTEMI
Unstable angina

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20
Q

What are the risk factors for ACS?

A

Modifiable:

  • Obesity and physical inactivity
  • Hypertension
  • Hypercholesterolaemia
  • Smoking
  • DM
  • Alcohol excess

Unmodifiable:

  • Age
  • Male sex
  • Genetic
  • Ethnicity
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21
Q

What are the signs and symptoms of ACS?

A 
Crushing, central chest pain radiating up neck and down left arm *diabetics and the elderly may not have chest pain
Dyspnoea 
Palpitations
Sweating
Nausea and vomiting 
Syncope

Pale and clammy
Often normal pulse (sometimes tachy), BP and O2 stats

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22
Q

What cardiac enzymes are measured?

A

Troponin (T or I) is the most sensitive and begins to raise from 3-12 hours after onset of pain with a peak at 24-48 hours and decline over 5-10 days

CK-MB rises after 3-12 of pain onset and returns to baseline 48-72 hours

LDH

Myoglobin levels rise within 1-4 hours which is sensitive but not specific to ACS

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23
Q

How are MIs localised on ECG?

A 
Inferior- II, III, avF-RCA**branchsupplies AVN so can cause complete heart block 
Septal- V1+V2-LAD
Anterior- V3+V4-LAD
Lateral- I, aVL, V5+V6-lCfx
Posterior- Tall R in V1+V2-lCfx+ RCA
Tall T wave
ST elevation (**in aVR is highly suggestive of 3 vessel or Left main stem disease)
T wave inversion 
Pathological Q (40ms wide >2mm deep)
**New LBBB in context of chest pain
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24
Q

How is ACS managed initially?

A 
Morphine
O2 (if <94%)
Nitrates (Glycerol trinitrate) sublignusally
Aspirin 300mg
Pasugrel (clopidogrel or ticagrelor)
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25
Q

How are STEMIs managed?

A

Purcutaneous Coronary intervention angioplasty +/- stent within 2 hours via radial or femoral catheter

Can drive 1 week after angioplasty and 4 weeks without one

Then:
Statin
Lifelong Aspirin + 1 mo of clopidogrel (lifelong if aspirin contraindicated) or tricagrelor 
ACEi
Beta Blocker to reduce heart rate
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26
Q

What is thrombolysis?

A

When PCI is not available for STEMI
(Also in stroke and PE)

Convert plasminogen to plasmin which degrades fibrin and breaks up clots

e.g. Alteplase
Tenecteplase
Streptokinase

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27
Q

When is thrombolysis contraindicated?

A

Can cause a bleed so…

  • Active bleeding
  • Recent haemorrhage
  • Recent trauma/surgery
  • Coagulation/bleeding disorders
  • Stroke < 3months
  • Intercranial neoplasm
  • recent head injury
  • Aortic dissection
  • Severe HTN
  • Pregnancy
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28
Q

How are NSTEMIs managed?

A

Antithrombin treatment:
FONDAPURINUX (Enoxaparin)If no risk of bleeding and no angiography in 24 hours

UNFRACTIONATED HEPARIN if angiography in 24 hours or high creatinine

Lifelong aspirin + 300mg of clipidogrel for 12 months

IV glycoprotein IIb/IIa receptor antagonists EPTIFIBATIDE or TIROFIBAN if high risk of CVS events + angiography within 96 hours

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29
Q

What is Angina?

A

MI caused by atheroma brought on by exertion and relieved by rest

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30
Q

What are the 4 types of Angina?

A

Stable: caused by exertion, relieved at rest
Unstable: increased frequency or severity on minimal exertion
Decubitus: precipitated by lying flat
Variant: prinzmetal’s- coronary artery spasm

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31
Q

What precipitates angina?

A 
4 Es
Exercise
Eating 
Emotion
Exposure to cold
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32
Q

How is Angina managed?

A
  • Lifestyle changes
  • Statin
  • Aspirin
  • B-B or CCB then combine (but not Verapapamil with BBlocker)
  • Nitrates
    Symptoms: spray subligually every 1/2 hour
    Prophylaxis: Regualr oral nitrate e.g. isosorbide mononitrate (can develop tolerence so take every 8 hours not 12 hours in standard release)
  • Ivabradine
  • PCI or CABG
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33
Q

What are the ECG changes that indicate thrombolysis or PCI?

A

ST elevation >2mm in 2 or more consecutibe anterior leads (V1-V6)

or

ST elevation > 1mm in >1 consecutive inferior leads (II, III, aVF, aVL)

or

New LBBB

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34
Q

What is coarctation of the aorta?

A

Stenosis in the aortic arch distal to the left subclavian artery

Hypertension proximally (upper limbs):

  • Dizziness
  • Headache
  • Neuro symptoms
Hypotension distally (lower limbs)
- Caudication

Collateral arteries between the pre-coarctation and post-coarctation aorta (e.g. intercostal and internal mammary arteries) enlarge and communicate between the aortic segments proximal and distal to the coarctation.

Enlarged intercostal arteries notch the inferior margins of te ribs detectable on XRAY.

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35
Q

What is an Atrial Myxoma?

A

Benign tumour of the heart

75% are in the left atrium

Surgery is curative

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36
Q

What are the features of Atrial Myxoma?

A

Mid diastolic murmur with ‘tumour plop’ in early diastole

Systemic:
- Dypnoea
- Fatigue
- Weight loss
- Fever
- Clubbing
Embolic (e.g. TIA)
Atrial Fibrillation
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37
Q

What is an Atrial Myxoma?

A

Benign tumour of the heart

75% are in the left atrium

Surgery is curative

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38
Q

What are the features of Atrial Myxoma?

A

Mid diastolic murmur with ‘tumour plop’ in early diastole

Systemic:
- Dypnoea
- Fatigue
- Weight loss
- Fever
- Clubbing
Embolic (e.g. TIA)
Atrial Fibrillation
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39
Q

What is Pulsus Paradoxus?

A

Systemic blood pressure falls by >10mmHg during INSPIRATION so the pulse is faint or absent when breathing in

CARDIAC TAMPONADE
Severe Asthma

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40
Q

What presents with Slow Rising/ Plateu pulse?

A

Prominant in carotids and brachials

AORTIC STENOSIS
LVF

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41
Q

What presents with Collapsing Pulse?

A

Waterhammer-Corrigan’s

Lift arn up vertically-hold muscular forarm, should feel tapping over muscles

AORTIC REGURGITATION
PDA
Hyperkinetic
e.g. exercise, fever, thyrotoxic, pregnancy

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42
Q

What presents with Pulsus Alternans?

A

Regular alternation of the arterial pulse

SEVERE LVF

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43
Q

What presents with Bisferiens Pulse?

A

Double pulse x2 systolic beats

MIXED AORTIC VALVE DISEASE

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44
Q

What presents with a Jerky Pulse?

A

HOCM

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45
Q

Where is Right Ventricular hypertrophy detected?

A

4th intercostal space in left parasternal area (right ventricular heave)

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46
Q

What is Transfusion Haemosiderosis?

A

Deposition of iron in heart (and endocrine organs) can lead to heart failure

47
Q

What is Cardiomyopathy?

A

Muscle becomes hard and thick and is sometimes replaced by scar tissue

48
Q

What are the Primary Cardiomyopathies?

A

Predominantly affect the heart

Genetic:
A.D
- Hypertrophic Obstructive (HOCM)
- Arrhythmic Right Ventricular Dysplasia (ARVD)

Mixed Cardiomyopathies:
Genetic predispositon to cardiomyopathy which is triggered by a secondary process
- Dilated Cardiomyopathy
- Restrictive Cardiomyopathy

Acquired Cardiomyopathies:

  • Peripartum
  • Takotsubo
49
Q

What is Hypertrophic Obstruction Cardiomyopathy?

A 
Defects in the genes encoding for CONTRACTILE PROTEINS 
- B-myosin heavy chain
- myosin-binding C protein
- cardiac troponin T
1/500
50
Q

What are the features of Hypertrophic Obstruction Cardiomyopathy?

A 
Asymptomatic
but:
- Dyspnoea
- Angina
- Syncope
- Sudden death
Arrhythmias -> ventricular
Heart failure: preserved ejection fraction 
Jerky pulse
Large 'a' waves on JVP
Double apex beat 
Ejection systolic murmur: increased during valsalva manouver and decreased when squatting
4th heart sound
51
Q

What are the features of Hypertrophic Obstruction Cardiomyopathy on ECG?

A
  • LV hypertrophy
  • Progressive T wave inversion
  • Deep Q waves
  • AF occasionally
52
Q

What are the features of Hypertrophic Obstruction Cardiomyopathy on ECHO?

A

MR SAM ASH

MR - Mitral Regurgitation

SAM - Systolic Anterior Motion of Anterior

ASH - Asymmetrical Septal Hypertrophy

53
Q

What is Arrhythmic Right Ventricular Dysplasia?

A

RV myocardium replaced by fatty and fibrofatty tissue

~50% have a desmosome gene mutation

54
Q

What are the features of Arrhythmic Right Ventricular Dysplasia on ECG?

A

ECG: V1-V3

  • T wave inversion
  • Epsilon wave - terminal notch in QRS
55
Q

What is Dilated Cardiomyopathy?

A

Dilated heart leads to systolic (with or without diastolic) dysfunction leads to enlarged heart with or without thickening

1/3 have genetic predisposition
no congenital, ischaemic or valve disease

56
Q

What are the features of Dilated Cardiomyopathy?

A

Reduced ejection fraction
Arrhythmias
Emboli
Mitral Regurgitation

57
Q

What is Restrictive Cardiomyopathy?

A

Walls of heart are rigid (not thickened) - restricted from stretching and filling

58
Q

What are the features of Restrictive Cardiomyopathy?

A 
Tiredness
Leg swelling
Shortness of Breath
Chest pain 
Fainting
59
Q

What are the Complications of Restrictive Cardiomyopathy?

A

Heart failure
Valve disease
Irregular heart beat

60
Q

What is Loeffer Endocarditis?

A

Restrictive cardiomyopathy affects the endocardium

WBC proliferation - specifically eosiniphils

61
Q

What is Peripartum cardiomyopathy?

A

Last month of pregnancy until 5 months post-partum

Older women, greater parity and multiple gestation

62
Q

What is Takotsubo?

A

‘Stress-induced’ e.g. traumatic events leading to chest pain (can mimic Anterior MI) and heart failure which is temporary

Transient, apical ballooning of the myocardium
Supportive treatment

63
Q

What are the Secondary Cardiomyopathies?

A

pathological myocardial involvement due to a generalised systemic disorder

e.g.

Amyloidosis
SLE
Haemachromatosis 
Sarcoidosis
Myotonic dystrophy
DM
Thyrotoxicosis
Acromegaly 
Alcohol 
Thiamine-VitB1-Wet Beri Beri
Coxsackie B
Chagas
64
Q

What are the Early Diastolic Murmurs?

A 
Aortic Stenosis
Pulmonary Stenosis
HOCM (loudest standing and during vagal, quietist squatting)
ASD
Fallot's
65
Q

What are the Pan Systolic Murmurs?

A

Mitral Regurgitation
Tricuspid regurgitaton
VSD ‘harsh’

66
Q

What are the Late Systolic Murmurs?

A

Mitral Valve Prolapse

Coarctation of the Aorta

67
Q

What are the Early Diastolic Murmurs?

A

Aortic Regurgitation
Pulmonary Regurgitiation
Graham-Steel

68
Q

What are the Pan Diastolic Murmurs?

A 
Mitral Stenosis (L lateral)
Austin-Flint
69
Q

What is a Graham-Steel Murmur?

A

Mitral Stenosis + Pulmonary HTN + Pulmonary Regurgitation

Mitral stenosis causes pulmonary HTN causes Pulmonary regurg

70
Q

When is S3 heard?

A

Ventricle filling
Normal in young and women <50

Pathological causes:

  • LVF e.g. in dilated cardiomyopathy
  • Contstrictive pericarditis - pericardial knock
  • Mitral Regurgitation
71
Q

When is S4 heard?

A

Atrial contraction against a stiff ventricle

  • HOCM (double apicle impusle due to palpable S4)
  • Aortic Stenosis
  • HTN
72
Q

What are the features of an Aortic Stenosis murmur?

A

Best heard RSE and radiate to carotids and apex on EXPIRATION

Syncope
Angina
Dyspnoea (exertional)

Associated with:

  • Slow rising pulse
  • Narrow pulse pressure
  • Heaving apex beat
  • Soft or absent S2
  • May have LVF w/ S3
73
Q

What are the causes of an Aortic Stenosis murmur?

A
  • Senile calcification
  • Congenital bicuspid valve e.g. in Turner’s
  • Rheumatic
  • HOCM
74
Q

What is the differentiating feature of an Aortic Sclerosis murmur?

A

Doesn’t radiate

75
Q

What are the features of an Aortic Regurgitation murmur?

A

Early diastolic
RSE or LSE sitting forward

  • Fatigue
  • SOB
  • Syncope
  • Exertional Dyspnoea
  • Orthopnea
  • Paroxysmal Nocturnal Dyspnoea

Associated with:

  • Collapsing pulse
  • Wide pulse pressure
  • Displaced apex
  • Quinke’s sign: pulsation in nails
  • Corrigan’s sign visible carotid pulsation
76
Q

What are the causes of an Aortic Regurgitation murmur?

A

Acute:

  • IE
  • Aortic dissection

Chronic:

  • CT disorders
  • Ank Spon
  • RA
  • Congenital
  • HTN
77
Q

What are the features of a Mitral Regurgitation murmur?

A

Best heard in apex and radiates to left axilla Expiration

  • Dyspnoea
  • Fatigue
  • Palpitations

Associated with:

  • AF
  • Displaced thrusting apex due to volume overload
  • Soft S1
  • LVF S3
  • Pulmonary HTN
78
Q

What are the causes of a Mitral Regurgitation murmur?

A 
Papillary muscle dysfunction e.g. after an MI
Dilated cardiomyopathy
Rheumatic 
Infective Endocarditis 
Congenital 
CT
79
Q

What are the causes of JVP ‘A’ wave changes?

A

Atrial Contraction

Large in:
Tricuspid Stenosis
Pulmonary Stenosis

Cannon in: contraction against a closed Tricuspid
Complete heart block
VT/Ectopics
Nodal Rhythm

Absent in:
AF

80
Q

What is the JVP ‘C’ wave?

A

Closure of the Tricuspid valve

81
Q

What are the causes of prominant JVP ‘X’ and ‘Y’ wave?

A

Fall in atrial pressure in ventricular systole

  • Constrictive pericarditis
  • Restrictive cardiomyopathy
82
Q

What is the cause of an absent ‘Y’ wave?

A

Cardiac Tamponade

83
Q

What is the cause of a giant JVP ‘V’ wave?

A

Filling of atria when tricuspid valve closed

Tricuspid regurgitation

84
Q

What are the causes of a raised JVP?

A

Constrictive pericarditis: Kussmaul’s: paradoxically raised in JVP during inspiration

Left ventricular free wall rupture (with pulsus paradoxus and reduced heart sounds)

Raised non-pulsatile JVP in SVC obstruction

85
Q

What is Anaphylaxis?

A

Severe lifethreatening and generalised type 1 IgE mediated hypersensitivity reaction

86
Q

What are the features of Anaphylaxis?

A

SERUM TRYPTASE HIGH FOR 12 HOURS

Capillary leak:

  • Urticaria
  • Erythema

Oedema:

  • Larynx
  • Lids
  • Tongue
  • Lips

Cyanosis
Wheeze
Laryngeal obstruction

87
Q

How is Anaphylaxis managed?

A

Secure airway, 100% O2

Adrenaline:
500mcg (0.5ml 1:1000) every 5 minutes into the ANTEROLATERAL MIDDLE 1/3 THIGH IM

Hydrocortisone
200mg

CLORPHENAMINE 10mg (continue 4mg/6hours if still itchy)

0.9% Saline 500ml over 5min up to 2 litres

88
Q

What is Pericardial Effusion and when does it occur?

A

Accumulation of fluid in the pericardial sack as a result of

Heart Failure

Vascular: Nephrotic syndrome
Idiopathic
Trauma
AI: Dressler's syndrome
Met: Uraemia
I
Neoplasm
D
89
Q

What are the features of Pericardial Effusion?

A
  • Dyspnoea
  • Raised JVP
  • Bronchial breathing
90
Q

What are the features on ECHO, CXR and ECG?

A

Enlarged ‘water-bottle heart’

Echo-free zone surrounding

Low QRS

Pericardiocentesis to determine bacterial cause

91
Q

What is Cardiac Tamponade and what can cause it?

A

Accumulation of pericardial fluid causing a rise in intercardial pressure, heart doesn’t fill, cardiac output falls

  • Biopsy
  • Transeptal rupture
  • Warfarin
  • Aortic dissection
92
Q

What are the features of Cardiac Tamponade?

A
  • Dyspnoea
  • Tachycardia
  • HoTn
  • Pulses Paradoxus (abnormally large fall in systolic BP + pulse wave amplitude during INSPIRATION)

ABSENT Y WAVE on JVP

Beck’s triad:

  • Low arterial BP
  • Distended neck veins
  • Muffled heart sounds
93
Q

What is Acute Pericarditis and what causes it?

A

Inflammation of the pericardium due to:

  • MI
  • CT diseases
  • Viruses e.g. Coxsackie, HIV, EBV, Flu, Varicella
  • Bacteria e.g. TP, Pnuemonia, Rheumatic, Staph and strep
  • Fungi
  • Drugs
94
Q

What are the features of Acute Pericarditis?

A

Central chest pain

  • Worse on inspiration
  • Worse lying flat
  • Better sitting forward
  • Pleuritic: central, sharp, stabbing
  • Dyspnoea, Tachypnoea
  • Hear PERICARDIAL FRICTION RUB
  • Fever
  • Tachycardia
95
Q

What are the diagnositic tests for Acute pericarditis?

A

WIDESPREAD SADDLE ST ELEVATION with PR depression Cardiomegaly if effusion

1/3 have raised troponin

96
Q

What is Constrictive Pericarditis?

A

Heart encased in stiff pericardium, cause usually unknown ?TB

97
Q

What are the features of Constrictive Pericarditis?

A
  • RHF signs: ascites, oedema, hepatosplenomegaly
  • Soft apex beat
  • Pericardial knock: LOUD S3

KUSSMAUL’S SIGN: Paradoxical rise in the JVP on inspiration or JVP fails to fall

JVP: PROMINENT X+Y

CXR: PERICARDIAL CALCIFICATION

98
Q

How is Acute Heart Failure managed?

A
  • oxygen
  • diuretics (furosemide-higher doses in renal failure)
  • opiates (diamorphine)
  • vasodilators
  • inotropic agents
  • CPAP
  • ultrafiltration
  • mechanical circulatory assistance: e.g. intra-aortic balloon counterpulsation or ventricular assist devices
99
Q

What is Bradycardia and how does it present?

A

HR <60bpm

  • Dizziness
  • Syncope
  • Palpitations
100
Q

What are the causes of Bradycardia?

A

SA Node Bradycardia (Sick Sinus Syndrome) due to fibrosis

  • SA Arrest
  • SA Block (1’, 2’, 3’)
  • Tachy-brady syndrome

AV Node block
- 1’, 2’, 3’

RBBB
LBBB
Bi and Trifasicular blocks

101
Q

What is SA Node Arrest?

A

SAN fails to depolarise so atria and ventricles don’t depolarise: NO QRS

102
Q

What is SA Node Block?

A

Depolarises but not conducted to the atria

1'-no changes
2'
- Type I Wenckeback
- Type 2
3' absent P ways
103
Q

What is Tachy-Brady syndrome?

A

SA Node dysfunction leads to SVT Tachyarrhythmia

Run of tachycardia followed by a run of bradycardia

Tachycardia can either be ESCAPE RHYTHMS or EXISTING TACHY (e.g. AF with SAN remodeling)

104
Q

What are the causes of AV Node Block?

A 
AI
Infective: endocarditis
Acute MI: INFERIOR RCA
Surgical: after ablation/valve surgery
AI: Ankylosing Spondylitis
Degenerative:
- fibrosis 
- calcification of nearby valves
Drugs: Digoxin, B Blockers, Ca channel blockers, anti-arrhythmics
105
Q

What is 1’ AV Node block?

A

Delayed conduction betwen the A+V through or around the AVN

  • Asymptomatic (pace if symptomatic)
  • P-R >5small squares (0.2s) but at a constant interval
  • Narrow QRS - Block within node
  • Broad QRS - Block in bundle of HIS
106
Q

What is 2’ AV Node block?

A

Partial conduction
Some make it through

MOBITZ TYPE 1 WENKEBACK
P-R lengthens until no WRS Black usually within node
Likely to progress

MOBITZ TYPE 2
No elongation in P-R but QRS dropped occasionally
e.g. every 3rd dropped = 3:1 block

PACE

107
Q

What is 3’ AV Node block?

A 
Complete heart block 
Complete dissociation of atrial and ventricular depolarisation 
No P-QRS relationship 
Narrow=Node
Broad= Bundle of His

PACE

108
Q

What is BBB?

A

Slowed conduction through ventricular system and higher

If one bundle is blocked impulse is transmitted to the other ventricle by non-specialised vascular tissue in between

109
Q

What are the causes of RBBB?

A
  • Ischaemia
  • P.E
  • Rheumatic heart disease
  • Myocarditis
  • Congenital heart defects
  • Cardiomyopathy
  • Cor Pulmonale
110
Q

What are the features of RBBB?

A

Wide QRS (>3sq, 0.12s)

Secondary R wave (Ri) in V1 and V2

ST changes are COMMON so hard to comment on ischaemia

SLURRED S in I/V5/V6

MORROW

111
Q

What are the causes of LBBB?

A
  • Cardiomyopathy
  • HTN
  • Coronary Artery Disease (acute anterior MI)
112
Q

What are the features of LBBB?

A

Wide WRS
R’ in
Absent Q in V5/V6

WILLIAM

113
Q

What are the fascicular blocks?

A

Bifasicular block:
- RBBB +R/L HEMIBLOCK
(RBBB +R/L axis deviation)

Trifasicular block:
BIFASICULAR + 1’ HB

114
Q

What are the hemiblocks?

A

Anterior MC : Left axis deviation

Posterior: Right axis deviation

FINALS (13 decks)

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