Cardiology & ECGs

Cardiology & ECGs

CSTC Plabinar Series: 11-12 Jan 2021

© Central Scotland Training Centre 2021

What is a PLABinar?

• Not just a lecture

• Active participation = active learning (better understanding & recall)

• Get out what you put in• Knowledge (lecturer covers high yield topics) Ⓚ

• Understanding (questions from the audience) Ⓤ

• Retention (questions from the lecturer) Ⓡ

• Application (audience answers high yield MCQs) Ⓐ

High yield items are marked in red throughout the PLABinar series

PLABinars – CSTC in action

• Cause(s) & Clinical pathophysiology

• Signs & Symptoms

• Tests

• Current management guidelines (UK based)

GMC Blueprint / High Yield topics

Chest pain / Palpitations Breathlessness / Oedema Miscellaneous

Arrhythmias Heart murmur Cardiac causes of syncope, dizziness and collapse

Acute Myocardial Infarction Valvular heart disorders Peripheral venous problems (see Surgery Plabinar)

• VTE/DVT• Varicose veins

Acute Coronary Syndrome Rheumatic heart disease

Angina Heart Failure

Acute pericarditis Cardiomyopathy Peripheral arterial disease (see Surgery Plabinar)• Aneurysms• Ischaemic limb• Occlusions

Cardiac tamponade High blood pressure

From birth (see Paediatrics Plabinar) Hypertension

Congenital heart disease Hyperlipidaemia/Cholesterol

ECG Basics Ⓚ

ECG Basics ⓀⓊ

ECG Basics

Please pair each part of the ECG to relevant answers & state ‘normal/abnormal’

1) PR interval A) 3.8 large boxes

2) QRS width B) 0.06 seconds

3) QT interval C) 0.16 seconds

4) RR interval D) 0.45 seconds

Ⓡ

ECGs & Arrhythmias – A Structured Approach

1. Pulse

2. QRS

3. Rotational axis

4. Sequence of ECG components

5. Treatment protocol

Arrhythmias

1. Pulse• Absent cardiac arrest algorithm

• Present clinical assessment of ABCDE (stable/unstable?)

Arrhythmias – Pulse (absent)

NO PULSE

Regular or Irregular?

Broad QRS

Pulseless VT

Regular

Ventricular Fibrillation

Irregular

Electrical activity

present?

Narrow QRSOr

Absent

PEA

Yes

Asystole

No

Shock + CPR (2 mins)(150 – 360 J biphasic)

Adrenaline + CPR (2 mins)(1 mg of 1:10,000)


NO PULSE


Broad QRS

Pulseless VT

Regular


Irregular

Electrical activity

present?

Narrow QRSOr

Absent

PEA

Yes

Asystole

No




NO PULSE


Broad QRS

Pulseless VT

Regular


Irregular

Electrical activity

present?

Narrow QRSOr

Absent

PEA

Yes

Asystole

No



Arrhythmias Ⓡ

A 68 year old man is found unresponsive. He has no central pulse and is making no respiratory effort. He is put on a cardiac monitor and the above rhythm strip is printed. What is the most appropriate initial response?

A) Give atropine 500mcg

B) Start chest compressions and give IPPV

C) Give adrenaline 1mg

D) Defibrillate at 150 Joules

Arrhythmias



Arrhythmias – Pulse (present)

Clinical status – Stable or unstable?

Assess using the ABCDE approach

Monitor SpO2 and give oxygen if hypoxic

Monitor ECG and BP, and record 12-lead ECG

Obtain IV access

Identify and treat reversible causes (e.g. electrolyte abnormalities)

Adverse features? Shock Syncope

Myocardial ischaemia Heart failure

Arrhythmias

Adverse Features mean they are UNSTABLE:• S Shock

• H Heart failure

• I Ischaemia (myocardial)

• P Passing out (syncope)

Arrhythmias



2. QRS• Rate - Fast or slow?

• Rise - Broad or narrow?

• Rhythm - Regular or irregular?

• Relationship - Previous parts (P, PR, P:QRS)

Arrhythmias

2. QRS• Rate: Fast or slow?

• 60 – 100 beats / minute is normal

• If rhythm is regular, rate = 300 / no. of large boxes across 1 RR interval

• If rhythm is irregular, rate = 300n / no. of large boxes across ‘n’ RR intervals

Arrhythmias




Ⓚ

Arrhythmias Ⓡ

This 58 year old man had this Lead II rhythm strip taken at rest. What is his heart rate?

A) 25 beats per minute

B) 75 beats per minute

C) 125 beats per minute

D) 175 beats per minute

Arrhythmias - QRS (slow)

Slow pulse

Ⓚ

Arrhythmias ⓇA 75 year old lady presents to your hospital in a collapsed state. Her respiratory rate is 20 breaths per minute. Her SpO2 is 98% on 15 litres/min of oxygen. Her pulse is present and CRT is 4 seconds. BP is difficult to pick up. She has two large bore IV cannulae in situ. This is her ECG. What is the best initial management for this rhythm?

A) Transcutaneous pacing

B) Start chest compressions

C) Give adrenaline 1mg

D) Give atropine 500 mcg

PAUSE

Arrhythmias




• Rise: Broad or narrow?• 0.12 seconds is normal (i.e. 3 small boxes)

• Broad complex > 0.12 seconds

• Narrow complex < 0.12 seconds (normal)

• Rhythm: Regular or irregular?• Mark 3 QRS complexes Move to the next 3 complexes

• Relationship: To make sense of the QRS, it is important also to look at:• P waves, PR interval (accessory pathways / BBB / heart block) and P:QRS ratio

Ⓚ

Arrhythmias – QRS (fast)Fast pulse

Ⓚ

Arrhythmias – QRS (fast)

• Unstable tachycardia• VT

• SVT

Ⓚ

Arrhythmias – QRS (fast BUT unstable)

Unstable tachycardia

Yes - UnstableSynchronised DC Shock*

Up to 3 attempts

Seek expert help !

Amiodarone 300 mg IV over 10-20 min

Repeat shock

Then give amiodarone 900 mg over 24 h

Assess using the ABCDE approach

Monitor SpO2 and give oxygen if hypoxic

Monitor ECG and BP, and record 12-lead ECG

Obtain IV access

Identify and treat reversible causes (e.g. electrolyte abnormalities)

Adverse features? Shock Syncope

Myocardial ischaemia Heart failure

Ⓚ

Arrhythmias – QRS (fast, narrow + stable)


• SVT

• Stable, narrow complex tachycardia (need to look at P morphology & P:QRS ratio)

• SVT

• Atrial fibrillation

• Atrial flutter

Ⓚ


Rate Rhythm P waves P: QRS rel’n

Sinus Tachycardia

100 – 180 Normal Normal 1:1

SVT 180 – 220(100+)

Regular Absent No P waves

Atrial Fibrillation

220 – 350 Irregular Ragged Unrelated

Atrial Flutter

> 350 Regular Saw tooth Fixed ratio (2:1 etc.)

Stable, narrow complex tachycardia

Ⓚ


Stable, narrow complex tachycardia

Seek expert help !

Is QRS narrow (< 0.12 s)?

Narrow

Narrow QRSIs rhythm regular?

Regular Irregular

Vagal manoeuvres Adenosine 6 mg rapid IV bolus

if no effect give 12 mgif no effect give further 12 mg

Monitor/record ECG continuously

Sinus rhythm achieved?

Yes No

Probable re-entry paroxysmal SVT: Record 12-lead ECG in sinus rhythm If SVT recurs treat again and consider

anti-arrhythmic prophylaxisPossible atrial flutter:

Control rate (e.g. with beta-blocker)

Probable AF: Control rate with beta-blocker or

diltiazem If in heart failure consider digoxin or

amiodarone Assess thromboembolic risk and

consider anticoagulation

Ⓚ

Arrhythmias – QRS (fast, broad + stable)


• SVT

• Stable, narrow complex tachycardia• SVT


• Atrial flutter

• Stable, broad complex tachycardia (need to look at BBB & PR interval)

• VT

• SVT with bundle branch block

• AF with bundle branch block

• AF with pre-excitation (WPW)

Ⓚ


• Bundle branch block (complete)• WiLLiaM MoRRoW

• LBBB = W in V1 / M in V6

• RBBB = M in V1 / W in V6

• Bundle branch block (incomplete)• Same as complete RBBB/LBBB BUT

• Narrow QRS (< 0.12s)

• Pre-excitation syndromes• Short PR interval

• QRS (ventricular) rate can be up to 300/min

• Lown-Ganong-Levine: narrow/normal QRS

• WPW (AVRT, AF, Atrial Flutter): broad QRS +/- delta wave

Ⓚ


Stable, broad complex tachycardia

Seek expert help !

Is QRS narrow (< 0.12 s)?

Broad

Broad QRSIs QRS regular?

Irregular Regular

Possibilities include: AF with bundle branch block

treat as for narrow complex Pre-excited AF

consider amiodarone

If VT (or uncertain rhythm): Amiodarone 300 mg IV over 20-

60 min then 900 mg over 24 h

If known to be SVT with bundle branch block:

Treat as for regular narrow-complex tachycardia

Ⓚ

Arrhythmias – QRS (fast)Fast pulse

Ⓤ

Arrhythmias ⓇA 25 year old man presents with spells of rapid pounding in his chest. He is completely conscious throughout the episodes with normal CRT, BP and SpO2. This was his ECG. Which is the most appropriate initial management?

A) Amiodarone

B) Adenosine

C) Cardioversion

D) Lidocaine

Arrhythmias



2. QRS• Fast or slow?

• Broad or narrow?

• Regular or irregular?

3. Rotational axis• Normal, right, left, superior?

Ⓚ

ECG Basics Ⓚ

ECG Basics Ⓚ

Arrhythmias

RIII>RIIRaVL>RI

Deep SIII

I / II Leaving each other LAD

I / II Returning towards each other RAD

Arrhythmias

What is the cardiac axis here? Is it normal?

Ⓡ

PAUSE

ECG Basics

4. Sequence of ECG components• Morphology: P, Q, R/S, T

• Interval: PR, QTc, ST

• Ratio: P:QRS

5. Treatment protocol

Ⓚ

ECG Basics Ⓚ

ECG Basics - Sequence of Components (P)

Best place(s) to look

• Lead II & V5

• Always +ve in II(as well as III & aVF)

• Not SR if not positive in Lead II

Ⓚ


What to look for – the 4 Rs

• Rate: atrial rate• Should match ventricular (QRS) rate if normal

• Absent in SVT

• Rise: 2.5 mm high, < 0.12s wide (all leads)• P mitrale: M-shaped (bifid) P wave in Lead II

• LAH

• P pulmonale: Peaky (tall) P waves• RAH

• Exacerbation of COPD

Ⓚ



• Rhythm: should be same as QRS• Should match ventricular (QRS) rate if normal

• Different if heart block

• Absent in SVT

• Rise: 2.5 mm high, < 0.12s wide (all leads)• P mitrale: M-shaped (bifid) P wave in Lead II

• LAH

• P pulmonale: Peaky (tall) P waves• RAH

• Exacerbation of COPD

Ⓚ



• Relationship:• PR interval

• Short in pre-excitation

• Long in heart block

• P : QRS ratio• 1:1 is normal

• 2:1, 3:1 or complete dissociation in heart block

• Top tips:• Inferior MI frequently assoc’d with conduction defects

Ⓚ


• Short PR = Pre-Excitation• WPW

• Long PR = Heart block• First degree

• PR fixed & prolonged (> 1 big box)

• Second degree (Mobitz Type I AV Block = Wenckebach)• PR increasingly prolonged until a QRS is missed

• Second degree (Mobitz Type II AV Block)• PR fixed but QRS drops (variably or in a fixed ratio P:QRS, e.g. 2:1)

• Third degree (Complete AV Block)• P is regularly present

• No relationship between P & QRS

Ⓚ


• Short PR = Pre-Excitation• WPW (vent. Pre-excitation)

• Prone to dysrhythmias• Orthodromic AVRT

• Antidromic AVRT


• Atrial flutter

• Rarely vent. dysrhythmias

• Narrow complex Rx• Similar to SVT

• Broad complex Rx• Unstable v. Stable

Ⓚ





Ⓚ





• Second degree (Mobitz Type I AV Block = Wenckebach)• PR increasingly prolonged until a QRS is missed

• Second degree (Mobitz Type II AV Block)• PR fixed but QRS drops (variably or in a fixed ratio P:QRS, e.g. 2:1)

• Third degree (Complete AV Block)• P is regularly present

• No relationship between P & QRS

Ⓚ

ECG Basics ⓇA 59 year old man presents to your emergency department with severe chest pain. An ECG is taken as shown. Which of the following abnormalities correctly relate to this gentleman’s problem?

A) Atrial fibrillation

B) Supraventricular tachycardia

C) Ventricular tachycardia

D) Second degree heart block

E) Third degree heart block

ECG Basics - Sequence of Components (QRS)

Where to look

• Start with Lead II (all except height & I/Ps), chest/limb leads (H+I/Ps)


• Rate: RR interval

• Rise: Early rise (delta waves)Broad or narrow (< 0.12s)Height (low/high voltage)Individual parts (Q, R, S)

• Rhythm: Regular or irregular

• Relationship: QTc, R/S, ST

Ⓚ


Narrow is Normal

Wide is Worrying• Patients Potassium (K+)

• Who WPW (pre-excitation)

• Present Pacemaker (vent.)

• Can Class I antiarrhythmics

• Be Bundle branch block

• Very Ventricular rhythms

• Trying Tricyclic antidepressant

Ⓚ


• Height: one limb lead > 5mm AND one chest lead > 10mm• If lower than this, its ‘low voltage’

Tamponade, Cardiomyopathy, COPD, PTX, Extensive MI, Obesity, Effusion

• If S WaveV1 or V2 + R waveV5 > 35mm, its ‘high voltage’Hypertrophy, BBB, normal in young, fit and slender people

• Affected by• Ventricular mass (hypertrophy)

• Ventricular size (enlargement)

• Distance between electrodes & heart

Ⓚ

ECG Basics - Sequence of Components (Q)

• Pathological in:• Myocardial infarction

• Left sided PTX

• Dextrocardia

• Perimyocarditis

• Cardiomyopathy

• Amyloidosis

• BBB, fascicular blocks

• Pre-excitation (WPW)

• Ventricular hypertrophy

• Acute cor pulmonale

Ⓚ

ECG Basics - Sequence of Components (R)

• R/S progression: should be V1 V5 then drop at V6

• Myocardial infarction, cardiomyopathy (HOCM v. Dilated), RVH v. LVH

• Dominant (RV1,V2 > S AND more than 5mm)Post. MI, RVH, RBBB, HOCM, Pre-excitation, P/L ischaemia/infarct, Dextrocardia, Situs inversus

• Reversed:LVH, Cardiomyopathy, Cor pulmonale, LBBB, Pre-excitation

Ⓚ

ECG Basics - Sequence of Components (S)

• Primary ST-T changesAbnormal repolarisationIschaemia, digoxin, K+, CCF, SVT

• Secondary ST-T changesAbnormal depolarisation repolarisationVentricular hypertrophy, BBB, Pre-excitn/RV-PM

Ⓚ

ECG Basics - Sequence of Components (S)

• If MI Symptoms!!!• Extensive ischaemia

• Malignant arrhythmia

Ⓚ

Arrhythmias – Sequence of Components (T)

Where to look

• II, V2, V3

What to look for

• Size

• Concordance

• Symmetry

• Direction

Ⓚ

ECG Basics (T)

Top tip• Men die earlier

• Woman are more balanced, stay apart and shorter

Rarely high (6, 8, 10 rule)• II < 6mm

• V2, V3 8mm (f.), 10mm (m.)

• Hyperkalaemia

• Early MI (hyperactue T-waves)

Ⓚ

ECG Basics ⓇA 50 year old man presents to the emergency department with chest pain. The following ECG was taken. What is the most likely diagnosis?

A) Inferior myocardial infarction

B) NSTEMI

C) Anterior myocardial infarction

D) Posterior myocardial infarction

E) Lateral myocardial infarction

Antiarrhythmic drugs - Overview Ⓡ

Understanding how the drugs work is good but knowing when to use them is better

Side effects etc. discussed in ‘Pharmacology’ Plabinar

Antiarrhythmic drugs - Selection Ⓡ

Chest Pain – Overview (Latest NICE Guideline) Ⓚ

Chest Pain – Medication Ⓚ

Ivabradine• Inhibits current pacemaker• So reduces HR• It is a ‘Cardiotonic’ drug• Use when -Blockers don’t

work)• Do not use in shock

Chest Pain – ACS Ⓚ(Overview)

Chest Pain – ACS Ⓚ(Latest UK/NICE Guidelines)

Chest Pain – STEMI (early management) Ⓚ

Chest Pain – NSTEMI/Unstable Angina Ⓚ

Acute Myocardial Injury - COVID Ⓚ(New topic may be coming into PLAB)

Cardiac Tamponade – Causes & pathophysiology

What is it?

• A life-threatening, slow or rapid compression of the heart due to the pericardial accumulation of fluid, pus, blood, clots or gas

Why does it happen?

• It is the result of inflammation, trauma, rupture of the heart or aortic dissection

Cardiac Tamponade - Causes

Common Uncommon

• Pericarditis*• Tuberculosis• Iatrogenic (invasive procedure-related,

post-cardiac surgery)• Trauma*• Neoplasm/malignancy (commonest)

• Collagen vascular diseases (SLE, RA, scleroderma)

• Radiation induced• Post-MI• Uraemia• Aortic dissection*• Bacterial infection• Pneumopericardium

* High yield

Ⓚ

Cardiac Tamponade – Signs and symptoms

• Tachycardia (initial sign)

• Beck’s Triad• JVP - Pronounced x descent and absent y descent• BP• heart sounds

• Pulsus paradoxus ( SBP > 10 mmHg during normal inspiration)

• May be absent in patients with markedly elevated LV diastolic pressures

Ⓚ

Cardiac Tamponade – Signs and symptoms

• Kussmaul sign• Paradoxical increase in jugular venous distention and pressure in inspiration

• Ewart sign / Pins sign• An area of dullness, with bronchial breath sounds and bronchophony below

the angle of the left scapula

• Dysphoria• Behavioural traits, e.g. restless body movements, unusual facial expressions,

restlessness, sense of impending death

• Low-pressure tamponade• In severe hypovolaemia, classical signs e.g.BP, pulsus paradoxus,

and jugular venous distention are less frequently seen

Ⓚ

Cardiac Tamponade – Tests and investigations

• ECG• Signs of pericarditis (especially low QRS voltages)• Electrical alternans

• CXR• Enlarged cardiac silhouette

• Echocardiography• Single most useful diagnostic tool• Identify effusion, estimate size/location/degree of haemodynamic impact

• CT and CMR / Cardiac catheterisation• Less readily available / rarely used to diagnose cardiac tamponade• Unnecessary unless Doppler echocardiography is not feasible

Ⓚ

Cardiac Tamponade – Current management

Remember to treat shock first (with IV fluids), if present!

Ⓚ

Acute Pericarditis – Causes & pathophysiology

What is it?

• Acute pericarditis is an inflammatory pericardial syndrome with or without pericardial effusion

Why does it happen?

• It may be caused by all categories of diseases, including infectious, autoimmune, neoplastic, iatrogenic, traumatic and metabolic

When does it happen?

• < 5 days if acute; 2-8 weeks if delayed (Dressler’s)

Ⓚ

Acute Pericarditis - Causes

Infectious Non-InfectiousViral (common) : Enteroviruses (coxsackieviruses, echoviruses), herpesviruses (EBV, CMV, HHV-6), adenoviruses, parvovirus B19 (possible overlap with aetiologic viral agents of myocarditis).Bacterial: Mycobacterium tuberculosis (common, other bacterial rare), Coxiella burnetii, Borrelia burgdorferi, rarely: Pneumococcus spp, Meningococcus spp, Gonococcus spp, Streptococcus spp, Staphylococcus spp, Haemophilus spp, Chlamydia spp, Mycoplasma spp, Legionella spp, Leptospira spp, Listeria spp, Providencia stuartii.Fungal (very rare ): Histoplasma spp (more likely in immunocompetent patients), Aspergillus spp, Blastomyces spp, Candida spp (more likely in immunocompromised host).Parasitic (very rare): Echinococcus spp, Toxoplasma spp

Autoimmune (common): erythematosus, Sjögren syndrome, rheumatoid arthritis, scleroderma), systemic vasculitides (i.e. eosinophilic granulomatosis with polyangiitis or allergic granulomatosis, previously named Churg-Strauss syndrome,Horton disease, Takayasu disease, Behçet syndrome), sarcoidosis, familial Neoplastic: Primary tumours (rare, above all pericardial mesothelioma). Secondary metastatic tumours (common, above all lung and breast cancer, lymphoma).Metabolic: Uraemia, myxoedema, anorexia nervosa, other rare. Early onset (rare): direct injury (penetrating thoracic injury, aesophageal perforation) and indirect injury (non-penetrating thoracic injury, radiation injury). Delayed onset: Pericardial injury syndromes (common) such as post-MI syndrome (fibrinous pericarditis), postpericardiotomysyndrome, post-traumatic, including forms after iatrogenic trauma (e.g. coronarypercutaneous intervention, pacemaker lead insertion and radiofrequency ablation).Drug-related (rare ): Lupus-like syndrome (procainamide, hydralazine, methyldopa, isoniazid, phenytoin); antineoplastic drugs (often associated with a cardiomyopathy, may cause a pericardiopathy): doxorubicin, daunorubicin, hypersensitivity pericarditis with eosinophilia; amiodarone, methysergide, mesalazine, clozapine, minoxidil, dantrolene, practolol, phenylbutazone, thiazides, streptomycin, thiouracils, streptokinase, p-aminosalicylic acid, sulfadrugs, cyclosporine, bromocriptine, several vaccines, GM-CSF, anti-TNF agents.Other (common) : Amyloidosis, aortic dissection, pulmonary arterial hypertension and chronic heart failure.Other (uncommon): congenital partial and complete absence of the pericardium.

* High yield

Ⓚ

Acute Pericarditis – Signs & symptoms / Tests

• History and Examination• Pleuritic chest pain (inspiration worse,

better on leaning forward): > 85 – 90%• Pericardial rub (on auscultation): <33%

• Investigations• ECG (new widespread saddle-shaped ST

elevation or PR depression): < 60%• Echo (pericardial effusion – new or

worsening): < 60%• Inflammatory markers: CRP, ESR, WCC• Myocardial injury markers: CK, TnT• CXR

Ⓚ

Acute Pericarditis – Tests Ⓚ

Acute Pericarditis – Current management

• Exercise restriction

• First line• Aspirin / NSAIDs

• Colchicine

• Second line• Low dose

corticosteroids

• Guide treatment time + response:• CRP

Ⓚ

Quiz ⓇYou are called to urgently assess a 60 year old gentleman who was admitted following an acute anterior myocardial infarction. His respiratory rate is 26 breaths per minute, SpO2 is 94% on 15L/min via facemask. His HR is BP is 70/40mmHg, CRT 5 seconds. He has a chest x-ray and ECG done (as shown). What is the most accurate description of his diagnosis?

A) Dressler’s Syndrome

B) Pneumonia

C) Cardiac tamponade

D) Acute pericarditis

E) Empyema

Heart Murmur

(+ bounding pulse, wide pulse pressure)

(associated with opening snap)

(apex)

(radiating to the axilla)

(crescendo / decrescendo)

(decrescendo)

Ⓚ

Crescendo / decrescendo (HOCM) – increase on valsalva and standing

Valvular heart diseaseAortic Stenosis Mitral Stenosis Pulmonary Regurg.

Cause Age (calcification)Cong. Bicuspid ValveRheumatic feverChronic renal probs

Rheumatic fever ToF RepairRoss ProcedurePS/valvuloplastyHx. of SBELV dysfunction/MS

Symptoms Long subclinical Hx.+Chest painHeart failureExercise intoleranceSyncopeTachypnoea/Dyspnoea

DyspnoeaOrthopnea

Dyspnoea Exercise tolerance

Tests (1st line) TTE, ECG ECG, CXR, TTE ECG, TTE, CXR

Current guidelines 1. SAoVR / TAVR2. SBE prophylaxis3. Anticoagulation

1. No therapy (NP)2. Diuretic3. Balloon valvotomy

Acute: medical Mx of CCF + Inotropes + SxChronic: specialised

Ⓚ

Heart Murmurs ⓇMrs Brown is a 50 year old lady who presents with breathlessness on minimal exertion. She had corrective surgery for cyanotic congenital heart disease when she was a young child, after a palliative operation during infancy. She does not remember much other than she was told she had a boot shaped heart. On examination of the praecordium, she has an early diastolic murmur with a parasternal impulse. Which of the following is your first choice of investigation?

A) Blood tests

B) ECG and Chest x-ray

C) Echocardiography

D) Cardiac catheterisation

E) None of the above

Rheumatic Heart Disease Ⓡ

What is it?

• Damage caused to the heart valves by rheumatic fever, which then do damage to the heart

Why does it happen?

• Complication of rheumatic fever

When does it happen?

• Any age but mostly children, therefore this topic will be covered in the Paediatrics Plabinar

Heart Failure - Pathophysiology Ⓡ

Heart Failure (Acute) – Diagnosis & Mx Ⓡ

Heart Failure (Chronic) - Diagnosis Ⓡ

Heart Failure (Chronic) - Management Ⓡ

Cardiomyopathies – Summary of Main Ones Ⓚ

Cardiomyopathies

What is it?

• Diseases of the heart muscle. There are different types:• Dilated cardiomyopathy (most common form)

• Hypertrophic cardiomyopathy (second most common form)

• Restrictive cardiomyopathy (rare)

• Other rarer types (not needed for PLAB):• Arrhythmogenic right ventricular cardiomyopathy (ARVC)

• Left ventricular non-compaction (LVNC)

• Takotsubo or ‘broken heart’ syndrome

Why does it happen?

• Sometimes unknown. Other causes: genetic, heart failure, cardiac arrest, connective tissue disease, autoimmune disease.

Ⓚ

Cardiomyopathies – Understanding them

• Dilated cardiomyopathy (DCM)This is when the muscle of the left ventricle becomes enlarged (dilated) and stretched. This makes the wall of the ventricle bigger but thinner, and so the muscle is weaker and less able to pump blood out of the heart. Although DCM can affect anyone, it can develop when a woman is pregnant, when it may be referred to as peripartum cardiomyopathy.

• Hypertrophic cardiomyopathy (HCM)This is when the muscle of the ventricle thickens and makes the ventricle smaller. The thickening means that the heart has to work harder to pump blood around the body. It can also block the flow of blood out of the heart.

• Restrictive cardiomyopathy (RCM)This is when the heart muscle becomes stiff and cannot relax properly, which makes it harder for the top chambers to fill with blood. The chambers then become enlarged and blood cannot flow properly.

• Arrhythmogenic right ventricular cardiomyopathy (ARVC), also called arrhythmic cardiomyopathy

When heart muscle cells are not joined together properly, and so they die and get replaced by scar tissue or fat. This makes the heart muscle stretched, thinner and weaker, making it less able to pump blood out of the heart.

• Left ventricular noncompaction (LVNC)When there is a problem with how the heart muscle develops in an unborn baby. The muscle cells do not compact (tightly pack) together as normal, which causes small indentations in the muscle and it appears spongy, affecting cardiac function.

• Takotsubo or ‘broken heart’ syndromeThis usually happens during a time of extreme stress (which gives it the name ‘broken heart’). The left ventricle becomes enlarged and weakened. It is often only temporary, and usually gets better with time.

Ⓚ

Cardiomyopathies – Clinical CareDilated Hypertrophic Restrictive

Cause Genetic (Aut. Dom.)Toxins (alcohol, doxo)Viral myocarditisPregnancy

Genetic (Aut. Dom.)Anderson-Fabry disease

Scar tissue in the heartAmyloidosisHaemochromatosisRadiation therapy

Symptoms DyspnoeaPeripheral oedema (inc ascites)FatiguePalpitations (arrhyth.)Chest pain (myo. Isch.)+S3 +/- S4, Mitral regurg., CCF

DyspnoeaDizziness or syncope (cereb. Isch.)FatiguePalpitationsChest pain+Dbl/displaced apex/carotid, ESM

Dyspnoea, coughSyncope, Peripheral oedema (inc ascites)Fatigue, loss of apetite, wtAmyloidosis symptomsChest pain, +JVP, Pulse vol

Tests (1st line is *)

ECG* (AF, LBBB, VEB, VT, VF)Exercise Test/Holter, ECHO, MRI

ECG*: LVH, RAH, LAD, Qinf/lat, AF/VT/VFECHO, Exercise Test/Holter, MRI

ECG*ECHO, MRI, Card cath, Biopsy, Bone Scan

Current guidelines

1. ACEI*/Ang2B*2. Beta blockers*3. Coag thinners4. Diuretics*/Digoxin*

1. Lifestyle management*2. Anticoagulation3. Beta blockers*4. Ca Channel blockers*5. Disopyramide*/Diuretics6. ICD (if arrhythmia) / Surgery

1. ACEI/Antiarrhythmics2. Beta blockers3. Coag thinners/Ca Channel blockers4. Diuretics*5. Vasodilators

Ⓚ

Hypertension – Overview Ⓚ

Hypertension – Current management Ⓚ

Hypertension – Current management Ⓚ

Hyperlipidaemia / Hypercholesterolaemia

Ⓚ

Syncope, Dizziness & Collapse Ⓚ

References & Further Resources

• National Institute for Health and Care Excellence

• European Society of Cardiology

• MIMMS

Documents

Cardiology & ECGs