Essential anatomy

• Sinus node

  • Generates impulses automatically by spontaneous depolarisation of its membrane

  • Pacemaker

  • Influx of sodium controls the depolarisation

  • The rate of depolarisation is controlled by: autonomic tone, stretch, temp, hypoxia, pH

• Atrial & ventricular myocyte action potentials

  • Different to sinus node cells

  • Arrival of AP opens Na channels resulting in a fast depolarisation

Cardiac Cycle

Cardiac arrhythmias

Bradycardia<60bpm

Tachycardia>100bpm

• Supraventricular

• Ventricular

Sinus rhythm

Mechanisms of arrhythmia production

Sinus bradycardia – slow automacity

Bradycadia due to AV block – abnormal conduction in the AV node

• Accelerated automacity

  • Reducing the threshold potential

  • Increasing the rate of diastolic depolarization

• Triggered activity

  • Myocardial damage can lead to oscillations in the transmembrane potential

  • These ‘after depolarisations’ may reach the threshold and produce an arrhythmia

Sinus bradycardia

Heart block

Atrioventricular block

First-degree block

Prolonged PR interval by more than 0.22s

Second-degree block

Some p waves occur but others do not

• Mobitz I block (Wenckebach)

  • Progressive PR interval prolongation until P waves fail to conduct

• Mobitz II block

  • Every now and then, there is a dropped QRS

• 2:1or3:1

  • Where every second or third P wave conducts the ventricles

3^rd degree (complete) block

When all activity fails to conduct to the ventricles

No relationship between P waves and QRS complexes

P waves ~90/min QRS ~36/min

Bundle Branch Block

Normal PR interval

Widened QRS complex

RBBB

Late activation of the right ventricle

MARROW

LBBB

Late activation of the left ventricle

WILLIAM

Supraventricular Tachycardias

Arise from the atrium or the AV junction

QRS is of a normal shape

Atrial fibrillation

When individual muscle fibres contract on their own

No P waves, irregular QRS although a normal shape

Atrial flutter

Rater >250bpm

Saw-tooth P waves

Often an associated block ~3:1

Ventricular Tachycardias

Broad QRS

T waves difficult to identify

Regular QRS~200bpm

Ventricular fibrillation

No pattern

Patient is likely to lose consciousness

Vaughn-Williams-Singh classification

Class I – sodium channel blockers

Class II – competitive beta-blockers

Class III – potassium channel blockers

Class IV – calcium channel blockers

Heart failure

When the cardiac output is inadequate for the body’s requirements

25-50% 5-year prognosis

1-3% of the general population, ~10% of the elderly

Alveolar oedema

Kerley B lines

Cardiomegaly

Dilated prominent upper lobe vessels

New york classification of heart failure
I	Heart disease present, but no undue dyspnea from ordinary activity
II	Comfortable at rest, dyspnea on ordinary activities
III	Less than ordinary activity causes dyspnea, which is limiting
IV	Dyspnea present at rest; all activity causes discomfort

Pleural effusion

Ischaemic Heart Disease

Angina Pectoris

Due to myocardial ischaemia

Acute coronary Syndromes

Unstable angina evolving to MI

Plaque rupture thrombosis inflammation

5/1000 per year

Differential diagnosis

Angina, pericarditis, myocarditis, aortic dissection, PE, oesophageal spasm

ACS with ST- ELEVATION (ACUTE MI)	ACS without ST-ELEVATION
O2 2-4L SaO2>95%	O2 2-4L SaO2>95%
IV acsess – FBC, U&E, glucose, lipids, cardiac enzymes	Morphine 5-10mg + metoclopramide 10mg
Aspirin 300mg	GTN
Morphine 5-10mg + metoclopramide 10mg	Aspirin 300mg
GTN – 2 puffs	Beta-blocker – atenolol 50-100mg/24hr
Primary PCI/ thrombolysis	Heparin – enoxaparin 1mg/kg/12h
Beta-blocker – atenolol 5mg	IV nitrate if pain continues
Consider DVT prophylaxis	Optimize drugs
Continue medications

.

Valvular Heart Disease

	Mitral		Aortic
	Regurgitation	Stenosis	Regurgitation	Stenosis
Cause	LV dilatation Annular calcification (elderly) Rheumatic Infective endocarditis Mitral valve prolapse Ruptured chordae tendinae Papillary muscle dysfunction Connective tissue disorders – Marfan’s Cardiomyopathy Congenital	Rheumatic Congenital Mucopolysaccharidoses Endocardial fibroelastosis Malignant carcinoid Prosthetic valve	ACUTE: Infective endocarditis Ascending aortic dissection Chest trauma CHRONIC: Congenital Connective tissue: Marfan’s Rheumatic fever RA SLE Seronegative arthropathies HTN	Senile calcification Congenital Rheumatic heart disease
Symptoms	Dyspnoea Fatigue Palpitations Infective endocarditis	Malar flush on cheeks – reduce CO	Exertional dysnoea Orthopnoea PND Palpitations Angina Syncope	Chest pain or exertional dyspnoea Angina Syncope Heart failure
Signs	AF Hyperdynamic apex RV heave	Low volume pulse AF Longer murmur = more severe	Collapsing pulse Wide pulse pressure Displaced hyperdynamic apex Capillary pulsations	Slow rising pulse Narrow pulse pressure Heaving, non-displaced apex
Murmur	Pansystolic radiating to axilla	Loud S1 sound Rumbling mid-diastolic murmur Loudest on expiration on left side	High pitched early diastolic murmur Expiration & sat forward	Ejection systolic Left sternal edge Radiates to the carotids
Investigations	ECG CXR – large LA & LV, mitral valve calcification & pulmonary oedema ECHO	ECG CXR – LA enlargement, pulmonary oedema, mitral valve calcification ECHO	ECG CXR – cardiomegaly, dilated descending aorta, pulmonary oedema ECHO Cardiac catheterization	ECG CXR: LVH, calcified aortic valve ECHO Cardiac catheter
Management	Control rate if fast AF Anticoagulate if: AF, Hx of embolism, prosthetic valve Diuretics may help Repair or replace valve ABX to prevent endocarditis	Control rate in AF Anticoagulate with warfarin Diuretics reduce preload & pulmonary congestion Balloon valvuloplasty Prophylactic oral penicillin against rheumatic fever	Reduce HTN – ACEi Surgery before LV becomes dysfunctional	2-3yr survival without surgery if Sx Valve replacement ASAP

	Tricuspid		Pulmonary
	Regurgitation	Stenosis	Stenosis
Causes	...

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