Cardiology Flashcards
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
Describe Q fever
Zoonotic bacterial infection with Coxiella burnetii
Common in sheep farmers
Describe the classification of endocarditis and the organisms which usually cause it
- Native valve endocarditis (NVE)
> Commonly caused by S. viridans, S.aureus or gram negative - Endocarditis in IVDUs (intravenous drug users)
> S. aureus, S. viridans or fungi - Prosthetic valve endocarditis (PVE)
> CoNS - S. epidermis, gram negative, fungi
Describe risk factors for endocarditis
- Increasing age
- IV drug use
- Male sex
- Specific for NVE: underlying valve abnormalities
> Aortic stenosis: caused by age-related calcification, calcification of congenitally abnormal valve or rheumatic fever
> Mitral valve prolapse
Describe rheumatic heart disease
- Caused by group A Strep infection (causes strep throat)
- Streptococcus pyogenes has an M surface protein
> Treatment of infection via immune system or antibiotics leads to release of M protein following bacterial lysis
> Anti-M antibodies produced against M protein - Through molecular mimicry, cardiac valves share similar antigenic structure to M protein
> So body’s own anti-M antibodies attack heart valves leading to stenosis or regurgitation
Describe the clinical features of endocarditis in IVDU
- Tricuspid valve endocarditis is more common than aortic or mitral
- Clinical features
> Acute: toxic presentation
» Progressive valve destruction and metastatic infection developing in days-weeks
» Commonly S. aureus
> Subacute: mild toxicity
> Presentation over weeks to months
> Rarely leads to metastatic infection; commonly Strep viridans or enterococcus
Describe the clinical features of endocarditis
- Early manifestations of infection
> Incubation period is 2 weeks; longer in PVE
> Fever + murmur is infective endocarditis until proven otherwise
> Fatigue & malaise - Embolic events
> Can take days-weeks to occur but seen earlier in acute endocarditis
> Small emboli: petechiae, splinter haemorrhages, haematuria
> Larger emboli: CVA, renal infarction
> Right-sided endocarditis (especially in IVDUs) - septic pulmonary emboli
- Late effects of infection
> Osler’s nodes: painful palpable lesions found on hands & feet
> Immunological reaction: splenomegaly, nephritis, vasculitis lesions of skin & eye, clubbing
> Tissue damage: valve destruction, valve abscess
Describe the diagnosis of infective endocarditis
- Blood cultures (3 sets from 3 different sites)
- Echocardiograph
> Transthoracic (TTE): non-invasive, transducer placed at front of chest, 50% sensitivity
> Transoesophageal (TOE): invasive, transducer placed in oesophagus, 85-100% sensitivity
- Duke criteria (positive if 2 major criteria or 1 major & 3 minor or 5 minor)
> Major:
> Typical organism in 2 separate blood cultures
> Positive echocardiogram or new valve regurgitation
> Minor:
> Predisposition (heart condition or IVDU)
> Fever >38ºC
> Vascular phenomena e.g. septic emboli
> Immunological phenomena e.g. Osler’s nodes
> Positive blood cultures not meeting major criteria
Describe the management of infective endocarditis
- Medical
> Antimicrobial therapy
» Bactericidal agents at high doses
» Duration of therapy: NVE is 4 weeks, PVE is 6 weeks
> > Streptococcus: benzylpenicillin +/- gentamicin
Enterococcus: amoxicillin/vancomycin +/- gentamicin
S. aureus MSSA: flucloxacillin +/- gentamicin
S. aureus MRSA: vancomycin +/- gentamicin
CoNS: vancomycin +/- gentamicin +/- rifampicin
- Surgical intervention
> If heart failure
> If uncontrollable infection e.g. abscess, persisting fever + positive blood cultures > 7 days, multi-drug resistant organism
> If needed to prevent embolism e.g. large vegetations or embolic episode
Define adult congenital heart disease and describe its prevalence
- Abnormal development within foetal heart resulting in birth defects
> Commonest birth defect: 1 in 145 live births
Describe the morphology of the heart
- Right atrium
> Sinoatrial node
> Broad appendage - Left atrium
> Narrow, long appendage - Right ventricle
> Trabeculated endocardium
> Insertion of chordae to interventricular septum
> Moderator band
> Tricuspid valve - Left ventricle
> Smooth endocardium
> Ellipsoid cavity
> Mitral valve (no septal connection)
Describe the pathophysiology and treatment of an atrial septal defect (ASD)
- Defect or hole in the atrial septum
- Types
> Secundum: most common, hole in the middle of the atrial septum
> Primum: more complex, partial atrioventricular septal defect (AVSD)
Describe ventricular septal defects, including complications and management
- If haemodynamically significant in early life can lead to pulmonary vascular disease
- Shunts left to right when in isolation - leads to left heart volume loading
- Examination: occasionally no murmur or pansystolic murmur
- Complications:
> Left ventricular failure
> Aortic valve regurgitation
> Right ventricular outflow tract obstruction
> Arrhythmias
> Pulmonary hypertension
> Eisenmenger syndrome - Management:
> Spontaneous closure
> Intervention - pulmonary band deployed, transcatheter closure device
> Surgery
Describe the clinical features of aortic coarctation
- Highly variable in severity - shelf-like or tubular stenosis in lumen of aorta
- Tends to form after left subclavian artery in a juxta-ductal position (forms where patent ductus arteriosus has been)
- Clinical features
> Bicuspid aortic valve
> Rib notching may be present on CXR due to retrograde flow from high pressure anterior intercostal arteries to low pressure posterior
> Collateral blood flow to bypass coarctation e.g. dilated ITA
Discuss the complications and management of aortic coarctation
Complications
- Upper body hypertension: difference between 2 arms
- Berry aneurysms
- Claudication
- Renal insufficiency
- Accelerated coronary artery disease
Management
- Surgical repair via thoracotomy: subclavian flap, end to end, jump graft
- Stent
What is meant by “Tetralogy of Fallot”?
Cyanotic congenital heart disease caused by deviation of part of ventricular septum
- Ventricular septal defect
- Overriding aorta
- Right ventricular outflow tract obstruction
- Right ventricular hypertrophy
Discuss the operative strategy for Tetralogy of Fallot including complications
- BT shunt: in child with low oxygen saturations (approximately surgery at 1 year)
> Repair involves closing the ventricular septal defect & opening the RV outflow tract and pulmonary valve
> This helps pulmonary arteries develop properly - Complete repair
Complications after repair:
> Significant pulmonary regurgitation; RV dilatation +/- dysfunction
> Arrhythmia: ventricular tachycardia
> Pulmonary arterial/branch PA stenoses
Describe the transposition of the great arteries and how this condition might be managed
- Great arteries (aorta & pulmonary artery) run parallel to each other instead of crossing over
- Diagnosis in utero (foetal echocardiography) & surgery within days of life
> Patent ductus arteriosus starts to close within first few days of life (allows mixing of circulation to sustain life) can be kept open by giving prostaglandins
- Management:
> Atrial switch: obsolete procedure where blood is switched at atrial level so oxygenated blood is pumped by right ventricle
> Arterial switch: trunk arteries are switched around from original position; aorta is attached to left side of circulation & coronary arteries are mobilised too
Describe the foetal circulation
- In utero oxygenation is by maternal placenta
- Pulmonary circulation is minimal and at high resistance
- Oxygenated blood returns to RA via IVC
- It then bypasses the RV/PA via the foramen ovale
> Of the blood that is pumped to the pulmonary arteries by the right ventricle, most passes to the aorta via the ductus arteriosus
Describe a univentricular heart and its treatment
- Heart with one functioning ventricle reliant on shunts for mixing of deoxygenated and oxygenated blood
- Treatment
> Aim of surgery is to create 2 functioning ventricles
> If not feasible then a Fontan circulation will be created
> Where there is a single functioning ventricle, this is used to support systemic circulation
> Plug in systemic venous return (IVC & SVC) directly to pulmonary vessels
> Leave oxygenated blood to return to single ventricular mass & pumped out through aorta
Describe the issues associated with Fontan circulation
- Pulmonary circulation is dependent on high systemic venous pressure and low pulmonary vascular resistance
- Anything that causes an imbalance can cause haemodynamic compromise
> Pulmonary embolism
> Arrhythmia
> Dehydration
> Bleeding
Describe heart failure and its causes
Failure of the heart to pump blood at a rate sufficient to meet the metabolic requirements of tissues
Causes
- Common
> Coronary artery disease (MI)
> Hypertension
> Idiopathic
> Toxins - alcohol, chemotherapy
> Genetics
- Less common
> Valve disease
> Infections - virus, Chaga’s
> Congenital heart disease
> Metabolic - haemochromatosis, amyloid, thyroid disease
> Pericardial disease e.g. TB
Discuss the main types of heart failure
- HF-rEF aka systolic HF
> Reduced ejection fraction
> Younger, male, often coronary aetiology - HF-pEF aka diastolic HF
> Preserved ejection fraction - Chronic (Congestive)
- Acute (decompensated)
Explain the pathophysiology of heart failure
- Myocardial injury (MI)
> Leads to left ventricular systolic dysfunction
> Perceived reduction in circulating volume and pressure
> Maladaptive neurohumoral activation
> SNS
> RAAS
> ET, AVP
> Natriuretic peptides
> Systemic vasoconstriction
> Renal sodium and water retention
List the signs and symptoms of heart failure
Symptoms
- Dyspnoea: orthopnoea, paroxysmal nocturnal dyspnoea, cough
- Ankle swelling: legs, abdomen
- Fatigue/tiredness
Signs
- Peripheral oedema: ankle, legs, sacrum, abdomen (ascites)
- Elevated JVP
- Third heart sound (S3)
- Displaced apex beat: cardiomegaly
- Pulmonary oedema: lung crackles
- Pleural effusion
Describe the New York Heart Association (NYHA) Functional Classification
- Class I: no symptoms, no limitation in ordinary physical activity
- Class II: mild shortness of breath + angina, slight limitation during ordinary activity
- Class III: marked limitation in activity due to symptoms even during normal activity, comfortable only at rest
- Class IV: severe limitations, symptoms even while at rest - mostly bedbound patients
List the investigations used for heart failure
- ECG: MI, left ventricular hypertrophy, rhythm, rate, QRS duration
- CXR: exclude lung pathology, pulmonary oedema
- Echocardiogram: chamber size, systolic/diastolic function, valves
- Blood chemistry: U&Es, Cr, urea, LFTs, urea (gout)
- Haematology: Hb (anaemia), RDW
- Natriuretic peptides: BNP, NT-proBNP
- Selected patients: coronary angiography, exercise test, ambulatory ECG monitoring, myocardial biopsy, genetic testing
Describe the diagnosis of heart failure
- Suspected heart failure: risk factors, symptoms/signs, abnormal ECG
- Measure NT-proBNP, BNP
- Echocardiography
- Confirmed heart failure
> Define heart failure phenotype based on LVEF measurement
Describe the medical management of HF-rEF
ALL patients:
- ACE inhibitor (ACE-I) e.g. enalapril or angiotensin receptor blocker-neprolysin inhibitor (ARNI) e.g. sacubitril valsartan
- Beta-blocker e.g. bisoprolol
- Mineralocorticoid receptor antagonists e.g. spironolactone
- SGLT2 inhibitor e.g. dapagliflozin
Additional medications:
- Diuretics
- If AF: anticoagulation
- IV iron: IDA
- Class II recommendation
> Ivabradine: sinus node inhibition (If inhibitor)
> Hydralazine + isosorbide dinitrate (vasolidator used in African-American populations)
Describe the mechanism of action of ARNIs
Angiotensin receptor blocker e.g. Candesartan, Losartan
> Blocks angiotensin II binding to AT1 receptor
> Reduces vasoconstriction, sodium/water retention and fibrosis/hypertrophy
Sacubitril blocks neprolysin , the enzyme which blocks natriuretic peptides
> Leads to vasodilation, natriuresis, diuresis, inhibition of pathologic growth/fibrosis
List the surgical approaches including devices used in the management of HF-rEF
- Cardiac resynchronisation therapy (CRT)
- Implantable cardioverter defibrillator (ICD)
- Left ventricular assist device (LVAD)
- Heart transplant
- CABG for atherosclerotic patients
- Total artificial heart
Describe cardiac resynchronisation therapy (CRT)
- Used in left bundle branch block (LBBB) - prolonged QRS to improve synchronisation between ventricles & improve CO
> Leads going to right atrium, right ventricle and left ventricle
> CRT-P: pacemaker; CRT-D: combined with defibrillator
> Higher NYHA class patients
Describe the mechanism of action of the implantable cardioverter defibrillator (ICD)
- Pacemaker that detects abnormal ventricular arrythmia
- Shocks into normal rhythm
- 1 lead into right ventricle
> Lower NYHA class patients especially in ischaemic aetiology e.g. MI
Describe the function of a left ventricular assist device (LVAD)
- Pumps blood out of the left ventricle into the aorta - continuous flow
- Risk of infection, clots
- Used as transition treatment for heart failure
Describe the management of the decompensating patient in acute heart failure
- Ultrafiltration: natriuresis
- Nitrates, nitroprusside, dobutamine: arterial vasodilation
> Reduce afterload (pressure the heart has to pump against)
> Increased inotropy - Nitrates, morphine: venodilation
> Reduce preload (venous return), reduce work - Furosemide: natriuresis - reduce fluid
- Dobutamine, dopamine, milrinone: increased inotropy
- Bilevel or continuous positive airway pressure (CPAP): preload reduction
Describe the symptoms associated with hypoperfusion and congestion in heart failure
Hypoperfusion
- Cold sweated extremities
- Oliguria
- Mental confusion
- Dizziness
- Narrow pulse pressure
Congestion
- Pulmonary congestion
- Orthopnoea/paroxysmal nocturnal dyspnoea
- Peripheral bilateral oedema
- Jugular venous dilatation
- Congested hepatomegaly
- Gut congestion, ascites
- Hepatojugular reflux
Describe the management of heart failure patients depending on their perfusion and congestion status
Warm-dry: well
- Adjust oral therapy
Warm-wet: congestion but adequate perfusion
- Vasodilators
- Diuretics
- Maybe ultrafiltration
Cold-wet: congested and hypoperfused
- Vasodilators
- Diuretics
- Inotropes
- Consider mechanical circulatory support
Cold-dry: hypoperfused, not congested
- Diuretics
- Inotropes
- Add mechanical support?
Describe the semilunar valves and some congenital abnormalities which may affect them
Aortic valves
- Lies between left ventricular outflow tract and aorta
- 3 cusps: trileaflet
- Right, left, non-coronary
> Bicuspid aortic valve: prone to premature dysfunction due to turbulent flow, associated with aortic abnormalities such as coarctation; can have a genetic component
Pulmonary valves
- 3 leaflets
- Lies between right ventricular outflow tract & pulmonary artery
Describe the atrioventricular valves
- Chordae tendinae attach papillary muscles to front aspects of leaflets - leading to closure of valves
- Mitral: lies between LA and LV
> 2 leaflets: anterior (more mobile, divided into 3, A1-A3); posterior (divided into 3 by clefts, P1-P3) - Tricuspid: AV valve, 3 leaflets, lies between RA & RV
List the causes of valvular heart disease
Valve leaflets
- Calcification
- Thickening
- Degeneration
- Infection
- Prolapse
Apparatus/annulus
- Annular dilatation
- Annular calcification
- Apparatus tethering/thickening/tupture
- Regional wall motion abnormality
Describe the causes, signs and symptoms of aortic stenosis
Causes: thickening, calcification, rheumatic valve disease, congenital
> Leads to increased LV cavity pressure, resulting in LV hypertrophy
Symptoms
- Dyspnoea
- Presyncope/syncope
- Chest pain
- Reduced exercise capacity
Signs
- Ejection systolic murmur
- Soft/quiet second heart sound
- Narrowed pulse pressure
- Heaving apex beat (LVH)
- Signs of heart failure
Do NOT give GTN - vasodilation can cause collapse
Describe the causes, signs and symptoms of aortic regurgitation
Causes: degeneration, rheumatic valve disease, aortic root dilatation, systemic disease e.g. Marfan’s syndrome, Ehlers-Danlos syndrome, ankylosing spondilitis, SLE; endocarditis
Symptoms: dyspnoea, reduced exercise capacity
Signs:
> Early diastolic murmur
> Increased pulse pressure
> Collapsing pulse
> Signs of heart failure
> Eponymous signs
» Corrigan’s: carotid pulsation
» Quinke’s: nail bed pulsation
» De Musset’s: head nodding
Describe the causes, symptoms and signs of mitral stenosis
Causes: rheumatic valve disease, congenital
> Leads to pressure overload, dilated LA
> Results in atrial fibrillation, pulmonary hypertension and secondary right heart dilatation
Symptoms:
- Dyspnoea
- Palpitation
- Chest pain
- Haemoptysis
- Right heart failure syndrome
Signs:
- Diastolic murmur
- Quiet second heart sound
- Heaving apex
- Signs of heart failure
Describe the signs and symptoms of mitral regurgitation
Mitral regurgitation leads to LV and LA dilatation, pulmonary hypertension, secondary right heart dilatation and atrial fibrillation
Symptoms
- Shortness of breath
- Palpitation
- Right heart failure symptoms
Signs
- Pansystolic murmur
- Quiet first heart sound
- Displaced apex beat
- Signs of heart failure
Describe the medical treatment for valvular heart disease
Medication is used to reduce symptoms by controlling heart rate and preventing arrhythmias
> Beta-blockers
Digoxin
Calcium channel blockers
Describe the surgical interventions used in the treatment of valvular heart disease
Valve repair
> Resect parts of redundant leaflet to reduce regurgitation and add a support ring
Valve replacement
> Ball & cage
> Bileaflet tilting disc prosthetic valve
> Metal valves: last longer, anticoagulation needed
> Tissue valves: don’t last long but no anticoagulation needed: resected animal valves made of pericardium
Other surgical options:
> Open heart surgery
> Minimal incision valve surgery
> TAVI (transcatheter aortic valve implantation) of a tissue valve in a self-expanding frame
> Mitraclip: patients not fit for open heart mitral valve replacement; pliable mitral valve leaflets are clipped & inserted
> Valvuloplasty
Define MI and outline the different types of MI there are
- Any elevation in troponin in clinical setting consistent with myocardial ischaemia
- Isolated troponin elevation does not equal MI
Different types:
- Type 1: spontaneous MI due to a primary coronary event (coronary artery rupture & thrombus formation)
- Type 2: increased oxygen demand/decreased oxygen supply
> Heart failure, sepsis, anaemia, arrhythmia, hypertension/hypotension
> Fixed atherosclerosis & supply-demand imbalance, or supply-demand imbalance alone - Type 3: sudden cardiac death
- Type 4a: MI associated with a PCI
- Type 4b: MI stent thrombosis documented by angiography
- Type 5: MI associated with CABG
Describe the signs and symptoms of a myocardial infarction
Symptoms
- Chest, back or jaw pain
- Indigestion
- Sweatiness, clamminess
- Shortness of breath
- None - diabetes/dementia
- Death
Signs
- Distressed patient
- Tachycardia
- Heart failure - crackles/raised JVP
- Shock
- Arrhythmia
- None
Describe the investigations used in acute MI
- Electrocardiograph
> Evidence of ST segment deviation - biomarker of myocardial ischaemia - Bloods
> Cardiac troponin: integral part of the cardiac myocyte, 3 types: TnI, TnT, TnC; release into blood stream is a marker of myocyte necrosis - CXR and echocardiogram
> Evidence of acute heart failure/left ventricular systolic dysfunction
> Coronary angiogram: coronary artery anatomy
Describe the HEART score for chest pain patients
History
> Highly suspicious, moderately suspicious, slightly suspicious
ECG
> Significant ST deviation or non-specific repolarisation disturbance, LBBB…
Age
> 65y
> 45-65
< 45y
Risk factors
>1-3 from the following: hypercholesterolaemia, hypertension, diabetes, smoking, family history, obesity OR history of atherosclerotic disease
Troponin
Describe non-coronary causes of elevated troponin
Causes of type 2 MIs
- Acute congestive heart failure
- Tachyarrhythmias - SVT, AF, VT
- Pulmonary embolism
- Sepsis
- Apical ballooning syndrome (Takotsubo cardiomyopathy)
- Anything that stresses the heart: critically unwell patient
Chronic elevation of troponin
> Renal failure, chronic heart failure, infiltrative cardiomyopathies e.g. amyloidosis, haemochromatosis, sarcoidosis
Describe the pathophysiology of a type 1 MI
- Rupture of the plaque exposes the subendothelial tissue triggering thrombus formation
> This blocks the arterial lumen and restricts blood flow acutely - ST elevation indicates complete blockage; if untreated it will completely infarct
> Reciprocal ST depression is characteristic of MI
State the coronary arteries which may be blocked in a myocardial infarction depending on its location
- Inferior STEMI: RCA (right coronary artery - mostly) or LCx (circumflex)
- Posterior STEMI: LCx (mostly) or RCA
- Lateral STEMI: LCx
- Anteroseptal STEMI: LAD (left anterior descending)
Describe the ECG features seen in a posterior infarct
- ST elevation not seen due to location
> Anterior leads are directly opposite & will see the opposite of any current generated at the posterior wall
> Posterior ST elevation = anterior ST depression
> Do posterior ECG
Describe the management of acute coronary syndrome
- STEMI
> ABCs + put in ambulance attached to defibrillator
> Oxygen if hypoxic (< 94% O2 sats)
> Aspirin 300mg PO
> Unfractionated heparin 5000U IV
> Morphine 5-10mg IV, GTN infusion 2nd line
>Anti-emetics
> Clopidogrel (ambulance)
> Ticagrelor (hospital)
> Activate PPCI team
> Reperfusion therapy:
> > Primary percutaneous coronary intervention (PCI) if <120 mins
- Transfer patient to cath lab rapidly, use transradial approach, insert catheter wire with balloon & deploy stent
> If not eligible - thrombolysis IV (alteplase, tenecteplase) + fondaparinux
Monitor in Coronary Care Unit for complications of MI
Drugs for secondary prevention
> ACE inhibitors
> Beta blockers
> Statins
> Eplerenone
> Aspirin (lifelong) / clopidogrel (6 months to a year)
» Shorter duration of anti-platelets if elderly, falls risk, GI bleed, major malignancy
> Echocardiogram for LV function & cardiac structure
Cardiac rehabilitation
If left ventricular systolic dysfunction at >9 months consider primary prevention ICD
Describe the complications associated with myocardial infarction
- Arrhythmias
> VT/VF - DC conversion
> AF - Heart failure
> Diuretics, inotropes, vasodilators - Cardiogenic shock
> Intra-aortic balloon-pump, ventricular assist device - Myocardial rupture
> Septum - VSD - surgery
> Papillary muscle - mitral regurgitation - surgery
> Free wall - tamponade - usually fatal - Psychological
> Anxiety/depression
> Cardiac rehabilitation
Describe the GRACE score risk model
Used for triage and prioritisation, predicts complications in hospital and post-discharge
> Low risk: discharge on medical treatment
Intermediate risk: discharge to be readmitted for angiogram
High risk: urgent inpatient angiogram
What is one of the main side effects of simvastatin?
Muscle pain caused by myositis, producing elevated creatine kinase, confusion and fever
What is the most accurate method for assessing left ventricular ejection fraction?
Cardiac magnetic resonance imaging
List the different types of bradyarrhythmias
- Sinus bradycardia
- Junctional bradycardia
- AV block
> Complete (third degree): complete dissociation betwwen P wave & QRS complex
> 2nd degree: every second P wave is non-conducted
>1st degree: prolonged PR interval but all P waves are conducted
Define the characteristics of junctional bradycardia as seen on ECG
- HR is 60bpm
- Absent P waves - no atrial activity due to SA node dysfunction or suppression due to high vagal tone
- Regular, narrow QRS complexes
Describe the NICE guidelines for the treatment of hypertension
Hypertension with type 2 diabetes: ACEi or ARB
Hypertension w/o T2DM, age <55 & not black African/African-Caribbean family origin
> ACEi or ARB
» ACEi or ARB + CCB or thiazide diuretic
»> ACEi or ARB + CCB + thiazide diuretic
»» resistant hypertension, consider adding low dose spironolactone (low potassium) or alpha blocker/beta blocker (high potassium)
Hypertension w/o T2DM, age >55 or black African/African-Caribbean family origin
> Calcium channel blocker (CCB)
» CCB + ACEi or ARB or thiazide diuretic
»> ACEi or ARB + CCB + thiazide diuretic
»» resistant hypertension, as above
Describe the signs of pericarditis on examination, including a syndrome which may appear after MI
ECG: widespread ST elevation, horseshoe shape
If pericardial effusion: cardiac tamponade
Auscultation: pericardial rub, muffled heart sounds
Dressler’s syndrome: pericarditis following an MI (pericardial effusion due to cardiac injury)
> Can present with chest pain, relieved by leaning forward
Describe the troponin levels and ECG changes associated with 1) unstable angina 2) NSTEMI 3) STEMI
1) Unstable angina
- Normal troponin
- Normal ECG; possible ST depression
2) NSTEMI
- Normal ECG
- ST depression
- T wave inversion
3) STEMI
- ST elevation
- Reciprocal ST depression
- T wave inversion
- New LBBB (anteroseptal MI)
Describe the ECG changes seen in a PE patient
S1 Q3 T3 pattern, sinus tachycardia, RBBB
