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Flashcards in Cardiology Deck (120):
1

Direction of View of ECG limb leads [Draw the Circle]

  • Lead I = 0
  • Lead II = 60
  • Lead III = 120
  • aVF = 90
  • aVR = -150
  • aVL = -30

 

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2

Placement & Direction of Precordial Leads

  • V1 = 4th ICS, R of Sternum
  • V2 = 4th ICS, L of Sternum
  • V3 = Between V2 & V4
  • V4 = 5th ICS, Left MCL
  • V5 = 5th ICS, Left Ant. Axillary Line
  • V6 = 5th ICS, Left MAL

V1 & 2 = RV

V3 & 4 = Septum & Anterior LV

V5 & 6 = LV Apex & Lateral LV

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3

R Wave Progression [What is it & Rationale]

  • For V1 & 2 [R< S]; V3&4 [R= S]; V5&6 [R> S]
  • Since LV > RV, depolarisations [represented by R waves] travel in the general direction of right to left
  • V1 & 2 represent RV hence small R wave as depolarisation is travelling away from these leads
  • V5&6 represent lateral LV & apex hence big R waves -> hence R wave progression from V1 to 6

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4

What does each component of the QRS complex represent?

QRS complex = Ventricular Depolarisation

  • Q = Septal Depolarisation [first small -ve after P]; NOT all leads have this; its direction = down + right since LBB innervated before RBB
  • R = Ventricular Depolarisation [first +ve after P]; ALL leads have this; direction = down + left since LV>RV -> size depends on which lead
  • S = -ve after R wave; NOT always present

 

5

What is the J-point on an ECG?

J = Junction

i.e. Beginning of repolarisation phase

The ST segment comes after the J-point

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6

Approach to ECG Interpretation

  1. Rate - Tachy/Brady
  2. Rhythm - relationship between P & QRS
  3. P wave - Atrial Abnormalities
  4. PR interval - Heart Blocks
  5. QRS complex - Axis Deviation, Ventricular Abnormalities, R/L Bundle Branch Blocks
  6. ST & T wave changes
  7. QTc interval

7

How to determine Heart Rate on ECG?

  • Best Method = 6x No of Full Beats on ONE ROW
  • Alternative = 300/no. of small squares between 2 QRS complexes

8

What is sinus rhythm?

What do the terms sinus arrhythmia and sinus arrest mean? 

  • = Rhythm under normal circumstances [each P followed by a QRS - 1:1]
  • Sinus arrhythmia = normal phenomenon whereby there is small increased HR during inspiration and small decrease during expiration [can also be felt during PE]
  • Sinus pause/arrest = SAN fails in its pacing function [pause = prompt recovery; arest = no recovery]

9

What is an Escape/Ectopic Rhythm on ECG?

  • What? - Pacemaker impulse originating from ectopic foci in either the atria, junction or ventricles
  • Why? - Mechanism to maintain impulse in sinus arrest or complete heart block
  • Patterns
    • Atrial - Normal QRS; Abnormal P
    • Junctional - Normal QRS; P usually buried
    • Ventricular - Wide QRS + abnormal shape

10

What is a Premature Beat on ECG?

  • What? - Ectopic pacemaker discharges impulse early; before next expected sinus impulse
  • Why? - Irritable ectopic focus competing with SAN
  • Patterns similar to escape rhythm; consecutive premature beats creates Tachycardias

11

How to determine Axis on ECG?

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12

How to observe Atrial Abnormalities on ECG?

Observe on lead II or aVF

Normal = RA depolarise before LA; both roughly equal in duration

RIGHT Atrial Abnormalities

  • RA depolarisation longer than normal; extends to LA depolarisation
  • P wave normal in duration (<3 small squares)
  • BUT Taller than normal (>2.5ss in height)

LEFT Atrial Abnormalities

  • LA depolarisation longer than normal; extends beyond normal P wave duration (>3ss)
  • P wave height is normal (<2.5ss) but may be notched (biphasic) due to increased duration

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13

How to observe Heart Blocks from ECG?

  • What? - Delay in AV conduction [@AVN or conductions pathways below]
  • Observed from - PR interval (normal = 3-5ss)
  • Types
    • 1o = Prolonged PR only; sinus rhythm
    • 2(Mobitz 1) = Progressively prolonged PR until a non-conducted P wave
    • 2o (Mobitz 2) = Sudden non-conducted P without progressive PR prolongation
    • 3o (Complete) = All SAN impulses are non-conducted; ventricular escape rhythm takes over [P & QRS not related]

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14

What are the Non-invasive Assessment Methods for Angina?

Functional

  • Exercise ECG (Treadmill) - Sn 45-50
  • SPECT (Thallium scan)
  • Stress ECHO - Sn85; Sp88
  • MRI

Anatomical

  • Multidetector CT Coronary Angiogram (gives coronary calcification score)

15

Results of Exercise Test that are Strongly Positive (3+3)

  1. ST Depression > 0.2mv at any stage usually upsloping @ 80ms beyond J-point
  2. ST Depression > 0.1mv during low workload
  3. ST Depression > 5mins on recovery
  4. SBP drop > 10mmHg
  5. Malignant arrhythmias induced
  6. High pre-test CV mortality risk

The more leads showing these changes; the more likely the patient has coronary stenosis

16

Contraindications of Stress ECG (7)

  • Known ACS - AMI within 2 days OR uncontrolled UA
  • Symptomatic Arrhythmias (tachy/brady) or those -> haemodynamic instability
  • LVOTO - Symptomatic severe AS & HOCM
  • Uncontrolled symptomatic HF
  • Acute PE, Myocarditis, AD
  • Severe HTN >200/110
  • Electrolyte abnormalities

17

Indications for Angiogram/PTCA in Angina Patients (3)

[PTCA = Percutaneous Transluminal Coronary Angioplasty]

  1. Medically refractory angina
  2. Post-infarct/-thrombolysis ischaemia
  3. Strongly positive stress ECG/Thallium scan

18

Indications for Statin Therapy (4)

  1. Known atherosclerotic CVD
  2. LDL-C >/= 4.9mg/dL
  3. DM pt. >40yo with LDL-C >1.8
  4. >40yo with LDL-C >1.8 PLUS 10yr CVS risk >7.5% 

19

Mechanism of new anti-anginal drugs (3 = TRI)

  1. Trimetazidine (X FA oxidation; cardioprotective)
  2. Ranolazine (Reduce Ca overload during diastole -> improve relaxation -> improve coronary blood flow )
  3. Ivabradine (blocks funny currents -> decrease HR & workload; only for HR>70)

20

What are the cardio-selective Beta-blockers and their contraindications (3)

Examples - Metoprolol, Bisoprolol

  1. Asthmatics
  2. Heart Block (2nd/3rd degree) or Bradycardia (<60bpm)
  3. (Frank) Heart Failure

21

Pharmacological Treatment for Angina

  • Lifestyle Modification - always remember
  • Improve Outcome - targets predisposing factors
  1. Aspirin - prevents thrombosis
  2. BB - decrease workload
  3. RF control - StatinACEI/ARB
  • Improve Symptoms
  1. Nitrates - vasodilator; increases supply & decreases demand
  2. CCB - mainly for spasm; can be combo with BB in HTN
  3. New anti-anginals

22

What does Acute Coronary Syndrome (ACS) include? How to differentiate the two NSTE-ACS entities?

ACS includes 3 diseases

  1. STEMI
  2. NSTEMI
  3. Unstable Angina

NSTEMI = has elevated cardiac enzymes;

UA = no elevated cardiac enzymes

23

Causes of Myocardial Ischaemia causing Chest Pain (4)

  1. Coronary Vessels - Atheroma, Thrombus, Vasospasm [CCB particularly useful]
  2. Hypertrophic Heart [inadequate coronary capillaries for LV mass] - HCM & HTN [-> LVH]
  3. Outflow Tract Obstruction - Aortic Valve Disease [esp. Acute AS/AR] & HOCM
  4. Others - Severe anaemia or thyrotoxicosis

24

DDx of Chest Pain Other than MI (4 groups)

  • Cardiac - PericarditisAortic Aneurysm [Dissecting / Ruptured]
  • Respiratory - PneumothoraxPulmonary Embolism, Pleurisy
  • Chest Wall - Rib fracture/mets, costochondritis, myalgia, herpes zoster 
  • Surgical - GERD, Oesophageal spasm/Oesophagitis, Oesophageal Rupture. Peptic Ulcer; Biliary Colic

25

Life Threatening Causes of Chest Pain (6)

[PET MAP]

  • Pulmonary Embolism
  • Esophageal Rupture
  • Tamponade
  • Myocardial Infarction
  • Aortic Dissection
  • Pneumothorax

26

Pathophysiology behind the progressive symptoms seen in NSTE-ACS (4)

Symptoms of NSTE-ACS are progressive and caused by

  • Non-occlusive thrombus on pre-existing ruptured plaque
  • Dynamic obstruction (coronary spasm)
  • Progressive mechanical obstruction
  • Sudden increased demand>supply

27

Features NOT suggestive of MI (4 - SOCR)

  1. S - Very localised pain to 1 finger
  2. O - Brief episode, lasting for seconds
  3. C - Pleuritic; associated with breathing/movement/palpation
  4. R - To lower limbs instead of L arm/neck/jaw/ back

28

Presentations of NSTE-ACS? (3)

Presentations include

  • Chronic angina with increasing frequencyduration or intensity
  • Angina at rest
  • New onset angina - severe & worsening

29

What is the first line screening for CAD? What is the purpose for screening?

10-year Cardiovascular Risk Score (e.g. Framingham, ACC/AHA) - Components include

  • Age & Gender
  • Lipids: HDL & Total Cholesterol
  • BP: SBP & any HTN treatment
  • Diabetes
  • Smoking

Purpose = Guide early treatment using Statins

30

Investigations for Acute Chest Pain (5)

  1. 12-lead ECG - ASAP
    1. ST elevation - admit immediately; prepare for reperfusion therapy [PT/APTT + baseline + NKDA -> aspirin + clopidogrel]
    2. No ST elevation - further evaluation
  2. If haemodynamically unstable -> ECHO (for possible PE/AD; followed by d-dimer & CTA if ECHO +ve)
  3. Cardiac enzymes - hsTnT (0h and 3h)
  4. Coronary CTA
  5. Others - Lipid profile, BG, CRP, ESR

31

Rule of Thumb for Diagnosis of Myocardial Infarction

2 out of 3 of

  1. Typical Chest Pain
  2. +ve ECG
  3. +ve Cardiac Enzymes

32

Algorithm for Evaulation of Patients with Suspected ACS

Key Points [for NSTE]

  • Admit + Manage ASAP if
    • ECG - ST +/- T wave changes
    • hs-cTnT> 99th percentile of ULN
    • Ongoing Pain
    • Haemodynamic abnormalities
  • If ECG not diagnostic + Normal hsTnT -> Observe for 12h from symptom onset

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33

Purpose of Early Risk Stratification in NSTE-ACS

  • Uses GRACE or TIMI scores to predict mortality of ACS patients on admission 
  • To determine whether immediate invasive tx (& transfer to PCI facility) is required
  • Poor prognostic factors include
    • Age > 65
    • CAD - >3 RFs or Known Hx or Aspirin use
    • Severe angina >2 ep w/in. 24hrs
    • ST deviation
    • + Cardiac marker

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34

Classical ECG Features of Acute MI

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35

What does ST Depression indicate?

Subendocardial ischaemia - i.e. demand > supply during exercise

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36

Cardiac Enzymes used in ACS investigation

  • Troponin - hs-cTnT has highest Sen & Spec; rises in 3-5hrs; peaks 24-48hrs; lasts days
    • Predicts future cardiac events in UA
    • TnI - Higher false +ve esp renal failure
  • CK-MB - peaks 24hr; returns to baseline earlier (2-3d); useful for detecting re-infarction
    • Change in CK/CK-MB more useful
  • Myoglobin - first marker to rise; non-specific; rapidly eliminated

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37

Diagnostic Algorithm for NSTE-ACS using Cardiac Troponin

Key Point

  • Re-test hs-cTnT after 3hrs if
    • At 1st test - Pain <6hrs & cTnT  OR
    • 1st test - cTnT > ULN
  • If 1st test highly abnormal hs-cTnT + worsening symptoms -> immediately manage

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38

Non-MI Cardiac Causes of Raised Troponin (5)

  1. Congestive Heart Failure
  2. Myocarditis/Pericarditis/Viral CMP
  3. Demand>Supply [Tachy/Bradyarrhythmia, Severe anaemia]
  4. Trauma [Surgery, RFA, Defibrillation]
  5. Takotsubo Cardiomyopathy

39

Non-MI Systemic Causes of Raised Troponin (5)

  1. Head - Subarachnoid Haemorrhage, Stroke
  2. Lungs - Pulmonary Embolism
  3. Kidneys - Renal Failure
  4. Sepsis
  5. Toxicity - Anthracyclines [e.g. doxorubicin]
  6. Blunt Chest Wall Trauma

CT may be required to r/o SAH & Stroke if hx/PE compatible

40

Role of ECHO in MI (3)

  1. Detects Abnormal wall motion
  2. Assess Ventricular wall function
  3. Detect Complications [​VSDPERV infarc, Ventricular Thrombus]

It is NOT routinely used to make MI diagnosis but useful to assess location, extent & complications AFTER diagnosis

41

Indications for Angiogram/PTCA in ACS

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42

Treatment Objectives in AMI & Options

(Acute, Remodelling & Late Phases)

Acute Phase - within 6h; limit MI size

  • Aspirin [Chew + Swallow if NKDA] & Clopidogrel
  • O2 supplement
  • Pain relief - TNG/BB/Opiods
  • Thrombolysis or PTCA

Remodelling Phase - limit dilatation of heart

  • ACEI
  • BB
  • PTCA

Late Phase - cardiac rehabilitation & prevention

  • Statin, ACEI/ARB, BB, Aspirin

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43

PCI vs Thrombolysis for ACS

  • PCI preferred if it can be done within 90 mins of admission
  • After 2 hours of AMI; PCI & Thrombolysis similar
  • Thrombolysis NOT useful if done after 4 hours of onset

44

Contraindications of Thrombolytic Therapy

Head

  1. Hx. of Intracranial haemorrhage
  2. Vessels – AVM, Aneurysm
  3. Malignant intracranial neoplasm
  4. Ischaemic stroke within 3 mo.
  5. Recent facial trauma/head injury

Others – Aortic dissection, Active bleeding/Bleeding tendency, Severe HTN

45

Ddx of Pleuritic Chest Pain (4)

[3P+I]

[Pleuritic Chest Pain = Worse with breathing]

Pulmonary Embolism
Pericarditis
Pneumothorax
Infection (Pneumonia, TB, Empyema thoracis)

46

Pathophsyiology of Pulmonary Embolism

  1. Thrombi starts in calf -> propagates
  2. Becomes proximal leg thrombi [above knee - popliteal, femoral or iliac]; must have this step to create sufficiently large thrombus
  3. Travels & Lodges in pulmonary arterial tree
  4. Increased pulmonary vascular resistance
  5. Reduced pulmonary blood flow & V/Q mismatch -> potentially Pulmonary infarct

47

Presentations of Pulmonary Embolism (DVT+3+4)

  • DVT: Calf pain, Leg swelling/erythema; Hx. of immobilisation [post-surgery, air travel]
    • NB: <30% patients have evidence of DVT
  • PE: Sudden onset of
    • Respiratory Symptoms (3)
      • Dyspnoea/Tachypnoea
      • Pleuritic Chest Pain
      • Haemoptysis
    • CVS/Systemic Symptoms (4)
      • Tachycardia
      • Shock
      • Hypoxia -> Cyanosis
      • Fever

48

List the Investigations for Pulmonary Embolism

  1. Clinical Picture Suspicious
  2. ECG & CXR - may have signs + r/o MI & Pneumonia
  3. If Highly Suspicious/Rapidly worsening - Proceed straight to Spiral CT/CT Angiogram
  4. Bloods
    • ABG - Decreased PaO2 despite supplement
    • D-dimer
  5. Imaging
    • LL Venous Doppler US
    • CT - Spiral or Angiography (CTA)
    • ECHO
    • V/Q Scan

49

ECG Features of Pulmonary Embolism

[Findings NOT sensitive or specific]

  • Sinus Tachycardia - most common
  • T wave inversion [V1-V4]
  • RAD
  • S1Q3T3 [classical] - Deep S [I]; Pathological Q & Inverted T [III]

50

CXR Signs in Pulmonary Embolism

[Frequently Normal/No significant abnormalities]

  • Subsegmental Atelectasis [Thin, horizontal opacities at one or both bases]
  • Elevated hemidiaphragm
  • Pleural Effusion
  • Wedge-shaped peripheral opacification  [usually lower lobes] representing pulmonary infarction

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51

D-dimer in Pulmonary Embolism

[How is it done? Accuracy? How is it used?]

  • How - Quantitative ELISA Assay
  • Accuracy
    • Highly Sensitive, Not Specific
    • Increased in sepsis, inflammation, CA
  • Utility
    • Normal (<500µg/l) result can rule out DVT/PE in LOW RISK patients
    • For HIGH RISK patients (e.g. elderly, hospitalised) normal result DOES NOT rule out DVT/PE
    • For elevated results -> further evaluate with duplex doppler US

52

Venous Duplex Doppler Ultrasound in DVT

[Accuracy? How is it interpreted?]

  • Accuracy
    • High Specificity & Sensitivity for DVT above kneeLower for DVT below knee
  • Interpretation
    • Positive test = reduced venous compressibility / non-compressible
    • ALL positive tests = rule in DVT
    • Negative tests rule out DVT ONLY if leg symptoms present
      • Possibility of calf/non-occlusive DVT

53

V/Q Scan in Pulmonary Embolism

[Accuracy, Indications, Contraindications, Interpretation]

  • Accuracy - Very sensitive; low specificity
  • Indications
    • Contraindicated to CT [Contrast allergy, Renal Dysfunction, Pregnancy]
  • CIs
    • Abnormal CXR/COPD
    • Suspect massive PE
  • Interpretation
    • Negative scan RULES OUT PE
    • High probability scan + High risk = Rules in PE
    • Other results = Non-diagnostic requires Duplex Doppler US/CT

54

Algorithm for Pulmonary Embolism Management

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55

Treatment Options for Pulmonary Embolism

  1. O2 Supplement if hypoxaemia/distress
  2. Pain relief - Paracetamol, NSAIDs, Morphine
  3. Acute anticoagulation [1 week] - SC LMWH [enoxaparin] or IV Unfractionated Heparin
    • ​​Get baseline CBC, PT/APTT, L/RFT
    • UFH - bolus then continuous infusion
    • Maintain aPTT @ 1.5-2x control
  4. Long Term anticoagulation [3-6mo.] - Warfarin
    • Overlap with LMWH/UFH for 5 days
    • Maintain INR @ 2 - 2.5x 
  5. For massive PE Thrombolysis [IV/Catheter-directed] or Surgical Embolectomy

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56

Prevention of Pulmonary Embolism

An IVC filter can be placed if indicated

  • Recent history of proximal DVT AND
  • Absolute contraindication for anticoagulation

57

Options for Pulmonary Embolism Prevention during Pregnancy

Non-pharmacological

  • Avoid immobility
  • Adequate hydration
  • Special elastic stockings

Pharmacological [in high risk patients/ previous DVT/PE] 

  • Anticoagulation throughout pregnancy + until 6 weeks post-partum [Warfarin can be used post-partum]
  • Avoid Warfarin during 1st trimester and after 36 weeks; use LMWH instead
    • Warfarin teratogenic; crosses placenta & anti-coagulates the fetus
    • Also applies to patients with active CA & high bleeding risk

 

58

Classification and Epidemiology of AF

  • Frequency – Paroxysmal [Self-terminating] vs Persistent [>7d] vs Permanent
  • Cause – Valvular vs Nonvalvular
  • Epidemiology – 1-2% population; M>F

59

Causes of AF

[5 Groups]

  • 50% acute AF have no identifiable cause; BOLD = Both acute & chronic causes
  • Neurological – SAH, Stroke
  • Cardiac – Any cause [MI, HTN, MV Disease, HF, Myo/Pericarditis, CMP, Cardiac Surg]
  • Pulmonary – COPD flare/Pneumonia, PE, OSA
  • Metabolic – Phaeochromocytoma, Thyrotoxicosis, Electrolytes
  • Drugs – Alcohol, Illicit drugs

60

Physical Signs in AF

  • Irregularly irregular pulse
  • Absent pulses – embolic complications
  • Loss of a wave in JVP
  • Signs of thyrotoxicosis [tremor, sweating, lid lag]

61

Pathogenesis of AF

  1. Ectopic foci produces atrial tachycardia (>400 bpm)
  2. Impulses conduct irregularly across atrial myocardium -> fibrillation
  3. AVN irregularly filters atrial impulses -> irregularly irregular ventricular response of <200 bpm
  4. Fine f waves on ECG baseline

62

Complications of AF (2)

  1. Heart Failure [tachycardia -> decreased cardiac output]
  2. Systemic embolisation [esp. stroke due to blood stasis -> thrombus formation]

63

Investigations for AF (3)

  1. Bloods – Electrolyte, TFT
  2. ECG – X p waves; replaced by fine f waves + irregular QRS
  3. ECHO – Underlying VHD, LAE, LVH; TEE for LA thrombus

64

Approach to Management of Acute AF

  1. Assess haemodynamic stability
    • Unstable → Urgent cardioversion
  2. Stable → Rate control [IV diltiazem/Dig/Metoprolol; goal HR<80]
  3. Anticoagulate [IV UFH]
  4. Consider Electrical/Pharm Cardioversion [>50% cases spontaneously cardiovert]
    • Empirical oral anticoagulation if ↑Stroke risk OR >48hrs for 4 wks

65

Modalities of Long Term Management of AF

[LT = Oral instead of IV]

  • Rate Control [Esmolol, Digoxin, CCB]
  • Rhythm Control [Class IC AAD – Flecainide, Class III – Amiodarone, Sotalol]
  • Anticoagulation (Warfarin or NOACs)
  • Non-Pharmacological – Ablation [RFA, Cath], Surgery

66

Rate vs Rhythm Control in AF

  • RateRequired for all patients for sx. control
  • Rhythm – ↑Cardiac function but ↑S/E; ind. if still symptomatic after rate control

67

What is the CHA2DS2-VASc score?

  • C - CHF
  • H - HTN
  • A2 - Age >75
  • D - DM
  • S2 - Stroke
  • V - Vascular disease
  • A - Age 65 -74
  • Sc - Female sex

Score >/= 2 requires warfarin/NOAC

68

What are the NOACs?

Novel Oral Anticoagulants (NOACs)

  • Thrombin inhibitor - Dabigatran; antidote available
  • Xa inhibitor - RivaroxabanApixaban, Edoxaban

69

What are advantages of NOACs c.f. to warfarin?

  • X require INR monitoring 
  • Less bleeding
  • Less drug-drug interactions
  • At least equal efficacy to warfarin

BUT not for AF secondary to valvular heart diseases/ prosthetic valve replacement

70

Atrial Flutter

[Pathophysi, ECG, Tx]

  • Re-entrant atrial loop → variable AV Block [AVN cannot conduct at 300bpm]
  • P:QRS = 2/3/4:1; Saw-tooth p waves
  • Anticoagulate & Tx as in AF

71

Pathophysiology of Marfan's Syndrome and Ehlers-Danlos Syndrome

Marfan's Syndrome

  • Mutation in fibrillin (FBN1) gene -> abnormal elastic fibre formation
  • AD pattern; 1 in 5 - 10,000; 25-30% new mutation

 

Ehlers-Danlos Syndrome (Vascular type; type IV)

  • AD pattern; 1 in 100,000
  • Type 3 collagen defect -> fragile BVs -> bleeding / aortic dissection/ aneurysm

72

CVS Complications of Marfan Syndrome (MAR)

  1. Mitral Valve Prolapse + MR
  2. Aortic Aneurysm Dissection
  3. Regurgitation (AR due to dilatation of aortic sinuses)

73

What are the features of Marfan's syndrome? (FAST Hollow Eyes)

Skeletal (5)

  • Fingers - Arachnodactyly + Joint Hypermobility
  • Arched Palate
  • Scoliosis & Tall Stature (Arm span > Height)
  • Hollow - Pectus Excavatum

Eyes (3)

  • Ectopia Lentis [also in EDS]
  • Myopia
  • Retinal Detachment

74

Diagnostic Criteria for Marfan's (with and without FH)

Ghent's Criteria

NO Family History 

Aortic root Z score >/= 2 (ECHO) PLUS either

  • Ectopia Lentis OR
  • FBN1 mutation OR
  • Systemic score >/= 7 pts (Wrist & Thumb Sign = 3pts; Pneumothorax = 2pt; Others = 1pt)

Family History of MFS PLUS

  • Aortic root Z score >/= 2
  • Ectopia Lentis
  • Systemic score >/= 7 pts

 

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75

Management of Marfan Syndrome (3)

  1. General
  • Regular clinical + ECHO FU
  • IE Prophylaxis
  • Avoid competitive sports/ weight lifting
  1. Medical - Beta-blockers [decrease rate of aortic dilatation & risk of dissection]
  2. Surgical
  • Elective replacement of ascending aorta [mortality 5-10%] IF progressive aortic dilatation >5cm
  • Resection & Graft in Types A AND B Acute Dissection in MFS (normally type B managed medically)

76

Marfan Syndrome and Pregnancy (2 issues)

  1. Inheritence - 50:50 risk of child inheriting MFS
  2. Increased Risk of Aortic Dissection if aortic root dilatation >4cm

Increased circulating volume [esp. 3rd trimester] -> Widened pulse pressure -> More stress to BVs

 

77

What is Aortic Dissection and How is it Classified?

  • Definition - Tear in aortic intima -> blood dissect into media
  • Stanford Classification
    • Type A - Involves ascending aorta
    • Type B - NOT involve ascending aorta
  • Chronicity
    • Acute - <2wks [mortality = 1% per hour for Type A]
    • Chronic - >2wks [mortality up to 80%]

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78

Causes and Pathophysiology of Aortic Dissection

  1. Hypertension [80%]
  2. Inherited Disorders of Connective Tissue
    • Marfan's, Ehlers-Danlos
  3. Congenital Bicuspid Aortic Valve
  4. Trauma

Pathophysiology

  • Collagen & elastin degeneration -> Cystic medial necrosis
  • Dissection can spread in either or both direction

79

Clinical Features of Aortic Dissection

[History & PE Findings]

History [Chronic can be asymptomatic]

  • Sudden onset severe tearing chest pain radiating to back [classical but not always]
  • Cx - SyncopeSOB, Sx of ShockHaemoptysis
  • Ischaemia - Chest pain (MI); Hemiplegia (Stroke); Abdominal Pain (Bowel ischaemia); Acute limb ischaemia; Paraplegia (Acute spinal infarct)

PE

  • BP - Hypo or Hypertension; Asymmetrical
  • Pulses - May be Absent or Asymmetrical
  • Murmur - New AR murmur [in Type A]
  • Weakness - UMN pattern

80

Investigations for Aortic Dissection

  1. CXR - abnormal in >80%
    • ​​Widened Mediastinum
    • Left pleural effusion [haemothorax]
    • Apical pleural effusion
  2. ECG - LVH + Assess for complications (e.g. MI)
  3. ECHO - TEE or TTE; can be done at bedside
  4. CT Angiography - Gold standard; Preferred over MRI
  5. Bloods - Lactate [ischaemic bowel], Troponin

81

Management of Aortic Dissection

Pharmacological [control BP to SBP 100-120]

  • Labetalol
  • Nitroprusside

Surgical - Resection & Graft

  • Indications
    • Type A
    • Type B if Marfan's, Rupture, Retrograde, End Organ Damage

Management of Cx

  • Drainage of tamponade
  • Aortic valve replacement in AR

82

Aortic Aneurysm

[Causes, Location, Clinical Features]

  • Localised dilatation of artery with diameter 1.5x > normal
  • Causes
    • Atherosclerosis
    • Infective [Staph., Salmonella, Syphilis]
    • Congenital - Bicuspid Aortic Valve, Connective Tissue Disorder
  • Location - Thoracic or Abdominal (90% infrarenal)
  • Clinical Features - Pain (Pressure effect), Emboli & co-morbidities (HTN, DL, PVD)

83

Investigation & Management for Aortic Aneurysm

Investigations

  • Bloods - CBC, Electrolytes, PTCT, PT/APTT, RFT
  • Abdominal US
  • CT/MRI

Management

  • Conservative - CVS risk reduction (HTN, DL, DM); frequent monitoring
  • Surgical [Open or EVAR] - if >6.5cm [5yr rupture risk = 20-40% if >5cm]

84

Stenosis vs Regurgitation

  • Stenosis → Pressure overload; affects chamber proximal to it
  • Regurgitation → Volume overload; affects chambers either side of it

85

What is the Rule of 1/3 for Bicuspid Aortic Valve?

  • 1/3 → normal
  • 1/3 → AS
  • 1/6 → AR
  • 1/6 → endocarditis → AR

86

Valve involvement of Chronic Rheumatic HD

[Autoimmune reaction to -haemolytic strep]

  • Mitral Commonest = MS > MS + MR > MR
  • Mitral + Aortic
  • Aortic
  • Tricuspid

87

Clinical Course and Pathophysiology of AR

  • Acute – Sudden ↓SV & ↑LVEDP → Pulmonary oedema +/- hypotension/shock
  • Chronic – ↑LVEDV → LV Dilatation to maintain compliance → Chronic volume overload clinically silent until CHF

88

Key Signs of AR (3)

  1. Early diastolic decrescendo murmur at LUSB increased with sit-up full expiration
  2. Wide Pulse Pressure >60mmHg – Regurgitation → lower DBP
  3. Displaced apex

89

Eponymous Classical Signs of AR (6)

  1. Austin-Flint murmur [mid-diastolic rumble @ apex]
  2. Corrigan’s Sign [Forceful pulsations of carotid arteries & collapsing pulse]
  3. Duroziez’s Sign [to-and-fro murmur over femoral]
  4. De Musset’s Sign [Head-bobbing with heartbeat]
  5. Pistol Shot Murmur of Traube’s [Over femoral]
  6. Quincke’s Pulse [Subungal capillary pulsations]

90

Causes of AR

[2 Groups]

Valve disease [40%]

  • Rheumatic [usually mixed AS/AR + MV]
  • Bicuspid aortic valve
  • IE
  • Valvulitis [RA, SLE, Drugs, RT]

Root disease [60%]

  • HTN
  • Aortic root dilation [AD, Marfan’s]
  • Aortic inflammation [Sero-ve arthritis (AS, Reiter’s), Syphilis, Giant-cell arteritis]

91

Investigations for AR

  • ECG – LVH, LAD
  • CXR – Cardiomegaly +/- dilated aortic arch
  • Bloods – Blood culture; VDRL
  • ECHO – LV size & function; Aortic root size; Severity of regurgitation

92

Management of Acute AR

[Usually AD or IE]

  • Pharm
    • ↓Afterload [Nitroprusside];
    • Inotrope [Dobutamine]
    • +/- Chronotrope [↑HR → ↓time for regurgitation]
  • Urgent surgery usually required

93

Management of Chronic AR

AV Repair/Replacement Indications

  1. Symptomatic
  2. Asymptomatic but severe [EF<50%; LV dilatation → LVESD>5cm; Cardiac surg anyway]
  3. May consider stress test [surg if +ve]

 

PharmVasodilator [ACEI/ARB, nifedipine] only in symptomatic/severe/inoperable

94

Causes of AS

  • Calcific – in >70yo; RFs = HTN, DL, ESRD
  • Congenital Bicuspid Aortic – 50% of <70yo AS
  • Rheumatic – with AR + MV disease

95

Key Signs of AS

  • Ejection systolic murmur @ aortic area with radiation to carotids
  • Heaving apex [in LVH]
  • Slow rising pulse
  • Decreased A2 [if severely calcified]

96

Pathophysiology and Presentations of AS

  • Asymptomatic until AV area < 1cm2
  • Angina – ↑Demand [LVH] + ↓Supply [LVOTO]
  • (Exertional) Syncope – Peripheral vasodilation + fixed CO → ↓Cerebral perfusion
  • LHF – Chronic LV pressure overload → LVH [Pul. oedema]

97

Investigations for AS (4)

  • ECG – LVH in late disease; LAE/LBBB
  • CXR – Cardiomegaly in late disease; AV calcification
  • ECHO – Estimate pressure gradient [sig if >40mmHg]; AV area [severe if ≤1cm2]; LVEF & Valve morphology
  • Cardiac Catheterisation – r/o CAD; more accurate gradient across AV

98

Dobutamine Challenge in AS

IndicationLow gradient AS [<30] with low EF

Differentiates between

  • Afterload mismatch – ↑SV & Gradient; X AVA change → AVR will ↑EF
  • Pseudostenosis – ↑SV; X Grad change; ↑AVA → Poor AV opening ∵Low CO
  • Limited reserve – X Changes in SV, Grad & AVA → AVR will prob X ↑EF

99

Indications for AVR in AS

  1. Symptomatic patients
  2. Asx + Severe [AVA<1; Grad >40] + EF<50%
  3. Asx + Severe + Other cardiac surg. OR Sx/↓BP with exercise OR +ve dobutamine challenge

100

Treatment modalities for AS apart from AVR

  1. Medical – BP control; +ve Inotropes [Digoxin] for ↓EF & HF
  2. Balloon AV Valvotomy – ↑AVA & ↓Grad but 50% restenosis by 6-12mo.; use as bridge to AVR/palliation
  3. TAVR [transcatheter AVR]
    • Ind: Medium/High Surg. Risk
    • ApproachTransfemoral/Axillary access → Balloon-expandable valve
    • Cx – Low CO, Paravalvular leaks, Complete HB

101

Pathophysi & Clinical Manifestations of MR

Acute MR [MI → chordae tendineae rupture or IE]

  • LV volume overload + ↑LA pressure → LHF & PAH → Pul. oedema & Cardiogenic shock [X time for LV remodelling]

Chronic MR

  • Asymptomatic for years
  • Progressive LHF → eSOB, Fatigue, Pul. HTN, AF

102

Causes of MR [4]

  • Valve Leaflet DegenerationMVP, IE, Rheumatic [usually + MS]
  • Chordae Tendineae Rupture – MVP, IE, Marfan’s, Trauma
  • Papillary Muscle DysfunctionMI
  • LV dilatation (Functional) – HF, HCM/DCM, Post-MI LV Remodelling

103

Key Signs of MR [4]

  • Pan-systolic murmur best heard at apex radiating to axilla
  • Displaced Apex
  • Soft S1 & S2; S3 may be present
  • Parasternal Heave [if severe PAH]

104

Investigations for MR [4]

  1. ECG – LVH, LAE
  2. CXR – ↑Cardio-thoracic ratio +/- pul. congestion
  3. ECHO – Assess MR severity, LV dilatation & function
  4. Cardiac Cath – Assess concomitant CAD before MV surg

105

Treatment for MR

Acute – Pharm + MV Repair/Replacement

  • ↓Afterload [IV nitroprusside]
  • Relieve congestion [Diuretics]
  • Inotropes [Dobutamine]

ChronicMV Repair/Replacement

  • Repair > Replace if MR not severe
    • Preserve Chordae & Papillary for LV function
    • Avoid LT anticoagulation
  • Indications
    • Symptomatic
    • Asx PLUS ↓EF OR LV dilatation

106

Pathophysi & Clinical Manifestations of MS

[MS → ↑LA pressure + PAH → RVH & RHF]

  1. Pulmonary Oedema + SOB → Orthopnoea, PND
  2. AF
  3. Embolic events – ∵Stasis in LA
  4. Pulmonary – Frequent bronchitis; Pulmonary hypertension
  5. Hoarseness [Ortner’s Syndrome] – LA compress RLN

107

Causes of MS

  1. Rheumatic [95%]
  2. Mitral annular calcification – esp. ESRD
  3. Congenital, IE, Autoimmune

108

Factors Predisposing Decompensation in MS

  1. Any Tachy [AF, Exercise]
  2. Chest infection
  3. Pregnancy [↑intravascular volume]
  4. Volume overload

109

How does AF lead to decompensation in MS

AF → ↑Ventricular rate → ↓Diastolic filling → ↓CO

110

Key Signs of MS

Mid diastolic low pitch murmur best heard @Apex in L lateral position with bell

  • ↑Duration of murmur = ↑Severity
  • Loudest during expiration after exercise
  • Loud S1
  • Opening snap – high pitched early diastolic sound
  • Tapping apex

Other Signs

  • AF – Irregularly irregular pulse
  • RHF – Ankle Oedema, ↑JVP
  • RVH – Parasternal Heave
  • PHTN – Malar Flush, Bil. Basal Crepitations

111

Investigations for MS

  • ECGLAE [p mitrale], RVH, AF
  • CXR – Dilated LA, Pul. congestion
  • ECHO – Estimate Gradient, MVA
  • Cardiac Cath – Assess concomitant CAD before MV surg

112

Treatment for MS

  • Medical – Anticoagulation for AF, Na restriction/diuresis, BB, Antibiotic prophylaxis [for rheumatic]
  • PMBC – Percutaneous mitral balloon commisurotomy
    • IndSymptomatic HF with MVA <1.5
    • Preferred for rheumatic HD
    • Pregnancy – indicated if NYHA III/IV; otherwise medical tx.
  • Surgical – MV repair if possible; otherwise replace

113

Signs of Mitral Valve Prolapse

  • Features of inherited disorders of connective tissue
  • Mid and late systolic clicks
  • Late systolic regurgitation murmur @ apex with atypical radiation

114

Should antibiotic prophylaxis be provided for MVP?

Not recommended anymore

115

Clinical Signs of TR

  • Giant v wave
  • Pulsatile liver
  • PSM best heard @ LLSB; + by inspiration; - by expiration
  • Parasternal heave
  • Oedema – LL and Ascites

116

Causes of TR

  • Primary – Rheumatic, RT, IE, Carcinoid/Tumours
  • Secondary [↑Common] – RVH due to LHF or PHTN [Cor Pulmonale, ASD] or MI

117

How is HF classified according to NYHA

  • Class 1 – X sx with ordinary activity
  • Class 2 – Sx with ordinary activity
  • Class 3 – Sx with minimal activity
  • Class 4 – Sx at rest

118

Types of HF

  • Low [↑common] vs High output
  • Left-sided [↑common] vs Right-sided OR BOTH
  • Systolic [↑common; ↓EF] vs Diastolic [X relax and fill; EF normal]

119

Causes of Left Systolic HF

[Most common type of HF; usually just referred to as HF]

↓Contractility ∵LV remodelling

  1. Ischaemia
  2. Valvular HD [Chronic MR, AR]
  3. Dilated CMP
  4. HTN

↑Afterload

  1. LVOTO – AS, HOCM
  2. Coarctation of Aorta

120

What is PA Catheterisation used for?

  • PA catheter = Balloon at catheter tip inflated → measures RA, RV, PA pressures and PCWP, an estimate of LA pressure and LVEDP
  • Estimation of diastolic filling of left heart (normal PCWP 2-12mmHg)

Indications

  • DDx of shock (cardiogenic vs distributive) and pulmonary oedema
  • Continuous CO monitoring,
  • Evaluate intracardiac shunt, PHTN, RHF, MR