Cardiology Flashcards
(89 cards)
Describe the stages of congestive heart failure
- Stage 1: redistribution, PCWP 13-18 mmHg
> Redistribution of pulmonary vessels
> Cardiomegaly - Stage 2: interstitial oedema, PCWP 18-25 mmHg
> Kerley B lines
> Peribronchial cuffing
> Hazy contours of vessels
> Thickened interlobar fissures - Stage 3: alveolar oedema, PCWP > 25 mmHg
> Consolidation
> Cotton wool appearance
> Pleural effusion: fluid within potential space between parietal and visceral pleura
» Seen as homogeneous lower zone opacity with a curvilinear upper border
Describe how impulses are conducted in the heart
- Sinoatrial node (SA node): near the entrance of the SVC
> Initiates heartbeat and determines heart rate: cardiac pacemaker
> Impulse from SA node spreads throughout atria, stimulating contraction - Impulse reaches atrioventricular (AV) node, which delays passage of electrical impulses to the ventricles
- AV node passes impulse into the atrioventricular bundle (bundle of His)
> divided into right and left bundle branches, which conduct impulses towards apex of heart - Signals are passed onto Purkinje fibres, which ascend through ventricular myocardium, triggering contraction
Describe the morphology of the ECG waveforms
- P wave: atrial contraction
- PR segment: time taken for impulses to travel from SA node to AV node
- QRS complex: firing of AV node and ventricular depolarisation
- ST segment: plateau in myocardial action potential - ventricular contraction (systole)
- T wave: ventricular repolarisation immediately before ventricular relaxation (diastole)
Describe the different chest leads used in the 12-lead ECG
- Anterior view: V1, V2, V3, V4
- Inferior view: Leads II, III, aVF
- Lateral view: Lead I, aVL, V5, V6
What is the QRS axis? What is its normal range?
The QRS axis is used to determine the average direction of ventricular depolarisation
> Normal QRS axis ranges from -30º to +90º, predominantly positive QRS in I and II
How do you determine heart rate on an ECG?
- 300 / number of large squares between each QRS complex
- Number of QRS complexes across ECG x 6
Describe the patterns of right axis and left axis deviation on an ECG
- Right axis deviation: +90º to +180º
> Predominantly negative QRS in I and aVL
> Can be pathological - cor pulmonale secondary to COPD - but also common in young, fit males - Left axis deviation: -30º to -90º
> Predominantly negative QRS in II and aVF
> Common in ischaemic heart disease or conduction problems
Describe the patterns seen in AV block on an ECG
- Complete heart block
> Complete dissociation between P wave and QRS complex
> Regular & slow rate - 2nd degree AV block
> Classic (Mobitz type 2): fixed prolongation of PR segment, non-conducted P wave with return to normal conduction at regular intervals
» 2:1 block indicates every second P wave is non-conducted
> Wenckebach (Mobitz type 1): progressive prolongation of PR segment
Describe the patterns seen in bundle branch block on ECG
- Right bundle branch block (RBBB) - MarroW
> Conduction through right bundle will be delayed so predominant conduction through left bundle on ECG
> Small positive deflection followed by larger deflection in V1 (M shape)
> Small negative deflection > large positive deflection > negative deflection in V6 (W shape) - Left bundle branch block (LBBB) - WilliaM
> V1: 2 negative deflections (1st smaller, 2nd deeper) - W shape
> V6: 2 positive deflections (1st smaller, 2nd larger) - M shape
Describe the algorithm used to identify tachycardias on ECG
- Fast & irregular
> Narrow QRS: AF
> Broad QRS: pVT or pre-excited AF; AF bundle branch block - Fast & regular
> Narrow QRS: sinus rhythm or supraventricular tachycardia
> Broad QRS: ventricular tachycardia or supraventricular tachycardia bundle branch block
Describe the ECG changes seen in pericarditis
- Clinical history not consistent with MI
- Concave ST elevation
- No specific territory (often global)
> No reciprocal change
> PR depression
Define atrial fibrillation as well as its symptoms
- Commonest sustained cardiac arrhythmia especially in the elderly
- Increases risk of stroke (5x)
- Symptoms
> Asymptomatic
> Palpitations
> Dyspnoea
> Rarely, chest pain or syncope
> Complications e.g. stroke (blood clots form in left atrial appendage)
Describe the investigations used in atrial fibrillation
- Irregularly irregular pulse
- Confirmed by 12-lead ECG
> Rate variable
> Irregular, narrow QRS
> No P waves - Echocardiogram
- Thyroid function tests: thyrotoxicosis can cause AF
- Liver function tests
Describe the risk factors for stroke and thromboembolism in non-valvular AF (CHA2DS2-VASc scoring system)
Major
- Previous stroke / TIA / thromboembolism
- Age > 75
Non-major
- Congestive heart failure / LV dysfunction
- Hypertension
- Diabetes mellitus
- Vascular disease
- Age 65-74
- Female sex
CHA2DS2-VASc
C: congestive heart failure/left ventricular dysfunction (1)
H: hypertension (1)
A2: age >=75 (2 points)
D: diabetes mellitus (1)
S2: stroke / TIA / thromboembolism (2 points)
V: vascular disease (1)
A: age 65-74 (1)
Sc: sex category (1)
Describe the management of atrial fibrillation
- Warfarin
- DOACs e.g. dabigatran, rivaroxaban
- Rhythm control
> Direct current cardioversion (persistent AF)
> Antiarrhythmic drugs (used in combination with a beta blocker)
> Class 1: sodium channel blockers (flecainide, propafenone)
> Class 3: potassium channel blockers - prolong action potential duration / QT interval; sotalol (beta blocker w/ class 3 activity), amiodarone
> Multichannel blockers e.g. dronedarone
> Catheter ablation: radiofrequency current - burning - or cryoablation - freezing with NO
(triggers for paroxysmal AF can be found in the pulmonary veins so pulmonary vein isolation can be curative)
Describe the different types of AF and the goals of treatment
- Paroxysmal - intermittent (prolonged ambulatory ECG used to detect)
- Persistent - requiring intervention to terminate the arrhythmia e.g. IV antiarrhythmic drug injection or DC cardioversion
- Permanent
Goals of treatment: target heart rate is <110/min or if still symptomatic, <80/min
> Patients without heart failure should be started on a beta blocker e.g. bisoprolol or atenolol, or rate-limiting calcium channel antagonist e.g. verapamil, diltiazem (digoxin as second-line)
Define atrial flutter and the changes seen on ECG
- Atrial flutter is related to atrial fibrillation - atrial rhythm is variable (regular or irregular) at 240-300bpm
- Characteristic sawtooth pattern seen in inferior leads (II, III, aVF)
- Re-entry around the tricuspid valve with variable ventricular rate
- ECG
> Regular narrow QRS
> Sawtooth atrial activity 300bpm
> Variable AV block
Define hypertension and its complications
- Persistently elevated arterial blood pressure > 140/90 mmHg
- Linear relationship between blood pressure and CV events such as MI, stroke, heart failure & PVD
Describe the 2 types of hypertension as well as their causes
- Primary (aka essential or idiopathic, 90-95%)
> Risk factors include
» Non-modifiable: age, gender, race, genetic factors
» Modifiable: diet, physical activity, obesity, excess alcohol, stress - Secondary (5-10%)
> Endocrine - Hyperaldosteronism, phaeochromocytoma, thyroid disease, Cushing’s syndrome
> Vascular
- Coarctation of aorta
> Renal
- Renal artery stenosis, renal parenchymal disease
> Drug
- NSAIDs, herbal remedies, cocaine, exogenous steroid use
> Other
- Obstructive sleep apnoea
Describe the pathophysiology of hypertension
BP = CO x TPR (cardiac output x total peripheral resistance)
- Defects in renal sodium homeostasis:
> Overactive renin-angiotensin-aldosterone system (RAAS) leads to salt & water retention
> Increase in total blood volume leads to increased cardiac output - Functional vasoconstriction:
> Decreased baroreceptor sensitvity
> Vascular tone may be elevated due to increased alpha adrenoceptor stimulation (overactive nervous system and RAAS system - vasoconstriction) - Defects in vascular smooth muscle growth and structure
> Growth factors such as angiotensin and endothelins can increase vascular smooth muscle leading to remodelling
Describe the investigations used in the diagnosis of hypertension
- Assessment:
> History e.g. risk factors, age of onset, medications, symptoms, family history and lifestyle
> Physical examination: BP both arms >2 readings on 2+ occasions, out of office BP measurement, BMI, examination of heart & lungs, auscultation of carotid, abdominal and femoral bruits, examination of thyroid gland and abdomen, palpation of the lower extremities (oedema and pulses), optic fundi examination, neurological exam & cognitive status assessment
> Investigations:
- Routine metabolic panel and lipids: hyperglycaemia or hyperlipidaemia
- Renal function: eGFR and creatinine
- FBC: Hb
- Urinalysis: ACR or PCR (albumin:creatinine ratio)
- ECG
- If investigations are unclear: echocardiogram & carotid dopplers, sleep study, phaeochromocytoma screen, TFTs, plasma renin/aldosterone, renal artery imaging
Describe the management of hypertension
- Lifestyle modification
> Education, sodium reduction, dietary approaches to stop hypertension (DASH) diet, weight loss, increased physical activity, limited alcohol consumption, smoking cessation - Antihypertensive drugs
> Diuretics: loop, thiazide, mineralocorticoid receptor antagonists e.g. spironolactone
> ACE inhibitors or angiotensin receptor blocker (ARB)
> Vasodilators: calcium channel blockers, beta blockers, alpha blockers
> Others: methyldopa, hydralazine, monoxidine - Device based therapies
> Renal sympathetic denervation - clinical trials
> Baroreflex activation therapy (BAT) - feasibility studies - Electrical stimulation of carotid sinus baroreceptor system
Describe infective endocarditis including the vegetation formed
- Infection of the endocardium
- Formation of a vegetation which results in damage to the cusps of the valves
> Most commonly mitral (followed by aortic, tricuspid & pulmonary valves) - The vegetation consists of a fibrin mesh, platelets, white blood cells, RBC debris and organisms
> Consists of a mass of different components forming a biofilm (adhere to foreign materials, treatment of infection often requires removal of the material) - Organisms communicate via quorum sensing: production of chemical messages which instruct other organisms to divide or become biochemically inert
List the organisms causing endocarditis
- Bacterial
> Gram positive
> Rods
> Cocci
- Staphylococci
> Staphylococcus aureus (coagulase positive staph) e.g. MRSA (methicillin resistant staph aureus) or MSSA (methicillin sensitive staph aureus)
> > Coagulase negative staphylococci (CoNS)
- Streptococci
» Streptococci viridans, enterococci
> Gram negative
> HACEK organisms: haemophilus, aggregatibacter, cardiobacterium, eikenella, kingella
> Enterobacteriales (Coliforms) e.g. E. Coli
> Pseudomonas aeruginosa
> Fungal, e.g. candida species - Candida albicans